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RC636  .B45  1 91 5    The  blood  and  its  di 


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THE  BLOOD 

AND  ITS 

DISEASES. 


HENRY  IRVING  BERGER,  M.  D. 


1915. 


Published  by 

BATTLE  &  CO. 
ST.  LOUIS.  MO. 


TABLE  OF  CONTENTS 

^.  Page 

Diseases  of  the  Blood: 

1 .  Simple  or  secondary  anemia 5 

2.  Progressive   pernicious    anemia 7 

3.  Chlorosis 9 

4.  Leukemia 20 

5.  Hodgkin's    disease 13 

6.  Splenic  anemia    (Banti's  disease) 15 

7.  Scurvy yi 

8.  Hemophilia 19 

9.  Purpura 20 

10.  "Blood  poisoning"    (Sapremia  and  Septicemia)...  23 

11.  Erythremia    (Vaquez's    disease — Polycythemia)  ...     2.5 
The  Blood: 

Definition,  color,  reaction,  composition 26 

Volume  index  and  blood  plasma 27 

Formed  elements,  enzymes,  gases 28 

Blood   pressure 28 

Hypertension  and  hypotension 29 

Specific   gravity 33 

Red   blood   cells:  — 

Morphology,  pathological   cells 34 

Counting 07 

01 

Color    index 3g 

White  blood  cells  :^ — 

Varieties 39 

Number,    classification 42 

Significance  of  leucocytosis 43 

Significance  of  leucopenia 44 

Counting  and  differential  count 44 

Preparation  of  blood  smears 45 

Staining 4g 

Hemoglobin ^9 

3 


TABLE  OF  CONTENTS— Continued 

Page 

Hemoglobinemia    and    hemoglobinuria 49 

Hemolysis 51 

Coagulation   of   blood 52 

Examination  of  blood  for  Bacteria  and  Parasites 55 

Tests  for  pus  in  blood.     (lodophilic  reaction) 67 

Blood  tests  in  Diabetes 68 

Griiber-Widal  reaction  in  Typhoid 69 

Bass  &  Watkin's  reaction  in  Typhoid 69 

Blood  tests  for  Syphilis i 70 

Abderhalden's  Sero-Diagnosis  of  Pregnancy 85 

Forensic  Medicine.      (Tests  for  Blood) 88 

1.  Morphological   test 89 

2.  Julius  Von  Kossa's  test 89 

3.  Van  Deen's  Guaiac  test 90 

4.  Schaer's    test 90 

5.  Phenolphthalein    test 91 

6.  Teichmann's  Hemin  Crystals 92 

7.  Spectroscopic   tests 92 

8.  Precipitin   reaction 95 

Differentiation  of  Blood  from  Iron  Rust 97 

Differentiation  of  Blood  from  Red  Paint 97 

Opsonins 98 

Hematemesis   (Gastrorrhagia)    100 

Hemoptysis 104 

Hematuria 106 

Hemorrhage  into  the  Brain 110 

Uterine  Hemorrhage  (Menorrhagia  and  Metrorrhagia) . . .   114 

Epistaxis 118 

Melcena    (Enterrhagia) 119 

"Ecthol" 123 


CHAPTER  I. 

DISEASES  OF  THE  BLOOD 


1.     SIMPLE  OR  SECONDARY  ANEMIA 

DEFINITION: 

Anemia  denotes  an  insufficiency  in  the  amount  of 
blood  especially  in  the  number  of  red  cells  and  in  the  per- 
centage hemoglobin. 

The  causes  of  all  secondary  anemias  are  known. 
The  most  frequent  cause  is  hemorrhage. 

In  simple  anemiia,  regeneration  of  blood  occurs  in  a 
normal  manner. 

CLASSIFICATION    AND    ETIOLOGY: 

1.  Surgical  Hemorrhage.     (Operations.) 

2.  Traumatic   Hemorrhage. 

(a)  External  or  visible  hemorrhage. 

(b)  Internal  or  concealed  hemorrhage. 

3.  Pathological  conditions  and  other  causes 

(a)  Hemorrhages   from   gen ito-uri nary  tract. 

(x)     Hematuria.     (See  p.  106.) 
(y)     Menorrhagia.     (See  p.  114.) 
(z)     Metrorrhagia.     (See  p.  114.) 

(b)  Hemorrhage  from  gastro-intestinal  tract. 

(y)     Hematemesis.     (See  p.  100.) 
(z)     Meloena.     (See  p.  119.) 

(c)  Hemorrhage  from  respiratory  tract. 

(y)     Hemoptysis.     (See  p.  104.) 
(z)     Epistaxis.     (See  p.  118.) 

(d)  Hemorrhagic  diathesis. 

(e)  Infectious  diseases. 

(f)  Diseases  associated  with  albuminuria. 

(z)     Acute  and  chronic  Bright's  disease. 

(g)  Chronic  suppurative  diseases. 


(h)     Toxic  Conditions: 

(y)     Mineral  poisoning  especially  lead. 

(z)     Acute  rheumatic  fever, 
(i)       Parasites: 

(x)     Malarial. 

(y)     Bothriocephalus  latus. 

(x)     Anchylostoma. 
(j)     Bad  hygienic  conditions  and  improper  food. 

DIAGNOSIS:     The  typical  blood-picture  is: 

1.  Reduction  in  percentage  hemoglobin  (oligochromemia) 
and  a  corresponding  decrease  in  the  number  of  red 
cells  (oligocythemia).  These  deviations  as  a  rule  run 
parallel. 

2.  Clianges  in  the  erythrocytes: 

(a)  Poikilocytosis  is  slight.  The  more  severe 
the  anemia  the  more  marked  is  the  altera- 
tion in  size  and  shape  of  the  R,  B.  C. 

(b)  Polychromatophilic  degeneration.  Varies 
greatly,  but  is  best  marked  after  hemorrhage. 

(c)  Nucleated  red  cells  (normoblasts).  Micro- 
blasts  also  found  especially  in  connec- 
tion with  malignant  tumors  of  the  intestinal 
tract. 

3.  Absence  of  leucocytosis.  But  after  hemorrhage  a 
"relative  leucocytosis"  occurs. 

4.  Eosinophilia,  if  anemia  be  due  to  parasites. 

SYMPTOMATOLOGY   of  Hemorrhagic  Anemia: 

1.  General  Remarks: 

Anemia  varies  with  rapidity  of  the  blood  lost 
and  individual  peculiarity  of  the  patient.  Bleed- 
ers recuperate  quickly.  Women  stand  the  loss  of 
blood  better  than  men.  If  one-half  the  total  vol- 
ume of  blood  be  lost  death  will  ensue. 

2.  Pallor.  The  more  blood  lost  the  greater  the  whitening 
of  the  skin  and  mucus  membranes  of  the  eyes  and  lips. 

3.  Dyspnea.     Respirations  increased. 

4.  Sweating  and  corresponding  thirst. 

5.  Vertigo  and  nausea. 


Shock  and  collapse  in  proportion  to  amount  of  blood 
lost.  The  same  symptoms  occur  in  concealed  as  in 
external  hemorrhage. 

Circulatory  symptoms. 

Pulse:  Weak  at  first  due  to  loss  of  volume 
of  blood  which  is  necessary  for  the  heart  to  work 
with.  Saline  infusions  restore  this  necessary  vol- 
ume. If  patient  becomes  exsanguinated  the  pulse 
becomes  imperceptible. 
Functional  murmurs: 

(a)  Hemic:  are  systolic  in  time,  untransmit- 
ted  and  heard  best  over  base. 

(b)  Continuous  venous  hum  (bruit  au  diable). 
By  pressure  over  jugular  vein  it  may  be 
made  to  disappear. 

Note:     When  the  anemia  improves  these 
murmurs  disappear. 

Amenorrhea.  In  chronic  cases  in  women  there  may 
be  a  suppression  of  menses. 


2.     PROGRESSIVE  PERNICIOUS  ANEMIA. 
(Addison's  Anemia — ^Biermer's  Disease.) 

DEFINITION. 

An  "idiopathic"  anemia  growing  progressively  worse 
characterized  by  abnormal  regeneration  of  the  blood  and 
by  hemolysis. 

It  usually  occurs  after  the  age  of  36. 

Although  the  Bothriocephalus  Latus  may  cause  such 
an  anemia  it  is  amenable  to  treatment. 

DIAGNOSIS.    "It  is  a  large  cell  anemia." 
(A)       BLOOD  PICTURE. 

Changes   in  the   red  cells. 

(a)  Normoblasts  and  megaloblasts. 

As  a  rule  the  megaloblasts  out-number 
the  normoblasts. 

"Crises"  of  either  of  these  forms  may 
occur. 

(b)  Poikilocytosis  very  exaggerated, 

(c)  Polychromatophllic  degeneration  extensive. 


(d)  Oligocythemia.  The  absolute  count  of  both 
R.  B.  C.  and  W.  B.  C.  is  reduced  from  20 
to  50%. 

Leucopenia.  The  reduction  in  the  white  count  runs 
parallel  with  the  reds. 

Hemoglobin  relatively  increased.  Color  index  is 
therefore  high  since  the  R.  B.  C.  are  decreased. 

(B)       SYMPTOMS.   The  disease  develops  insidiously  with: 

1.  Progressive  general  weakness  without  notice- 
able emaciation. 

2.  Gradually  increasing  profound  anemia.  Lemon- 
yellow,  puffy  face  associated  with  an  increase 
in  weight  is  very  characteristic. 

3.  Pronounced  cardiac  enfeeblement,  dyspnea,  ver- 
tigo, palpitation,  breathlessness  on  exertion  very 
marked.  Hemic  murmurs  may  occur  even  with- 
out valvular  lesions.  Advanced  cases  may  end 
up  with  fatty  degeneration. 

4.  Digestive  disturbances  with  periodical  attacks 
of  diarrhea  occur  in  50%. 

Nausea  and  vomiting  very  frequent. 

Diarrhea  may  be  associated  with  paroxys- 
mal pains  in  the  stomach. 

Depraved  appetite  and  yet  the  patient  lays 
on  weight  and  flesh. 

5.  Slight  edema  of  the  subcutaneous  tissues. 

Usually  first  perceptible  about  the  ankles 
and  feet. 

6.  Involvement  of  the  spinal  cord  causes: 

Tingling  and  numbness  of  the  extremities. 
Neuritic  pains  at  times. 

Some  show  features  of  lateral  sclerosis  with 
spastic  features  and  increased  reflexes,  while 

Others  resemble  tabes:  lightning  pains, 
girdle  sensation,  areas  of  anesthesia,  loss  of 
reflexes. 

7.  Subcutaneous  hemorrhages  in  the  form  of 
petechia  are  not  as  common  as  retinal  hemor- 
rhages. 

8.  Fever.     Slight  and  variable. 

9.  Periods  of  remittency.  But  the  symptoms  soon 
return. 

8 


3.     CHLOROSIS. 

DEFINITION. 

A  primary  anemia  without  cachexia,  occurring  ex- 
clusively in  young  girls  and  in  young  women,  charac- 
terized by  a  greenish  coloration  of  the  skin  and  a  great 
reduction  in  hemoglobin. 

DIAGNOSIS.     Confirmed  by  a  blood  examination. 

1.  Hemoglobin  tremendously   lowered. 

2.  Changes    in    red    cells: 

(a)  Pessary  or  ring-shaped  cells  predominate.  They 
are  called  "dropsical  cells." 

(b)  Macrocytes  and  some  microcytes  but  no  nu- 
cleated cells. 

(c)  Polychromatophilic  degeneration. 

(d)  Poikilocytosis  in  severe  cases  only. 

(e)  Total  blood  count  normal  or  perhaps  slightly  be- 
low. Usually  about  4,000,000.  Color  index  is 
therefore   low. 

3.  No  change  in  leucocytes. 

4.  Blood  plates  increased  in  number. 

.5.  Blood  plasma  increased.  Normally  the  corpuscular 
and  plasma  elements  of  the  blood  are  equal  in  vol- 
ume. In  chlorosis  the  plasma  is  raised  to  75%  and 
the  corpuscular  volume  reduced  to  25%. 

6.     Specific  gravity  reduced.     May  be  as  low  as  1030. 

SYMPTOMS. 

1.  Pallor.  Face  varies  in  color  from  a  pale  yellow  to  a 
greenish  hue.  The  swelling  under  the  eyes  gives  the 
patient  a  "nephritic"  appearance. 

2.  Stomach  symptoms. 

(a)  Depraved  and  perverted  appetite. 

(b)  Hyperacidity  with  or  without  gastric  ulcer. 

(c)  Obstinate  constipation. 

3.  Neuralgias: 

(a)  Occipital  and  supraorbital. 

(b)  Gastralgia  and  intercostal  neuralgia. 

4.  Amenorrhea. 

5.  Palpitation  very  prominent  in  many  cases. 

9 


PHYSICAL  SIGNS. 

1.  Tissues   pit  on   pressure    (edematous   infiltration), 

2.  Systolic  functional  murmurs  which  disappear  as  soon 
as  the  disease  is  cured.  Murmur  is  heard  best  over 
pulmonary  artery  but  is  not  transmitted,  and  second 
pulmonic  sound  is  not  accentuated. 

The   bruit-au-diable    is    heard    over    the     sterno- 
clavicular articulation. 

Rapid  heart  and  rapid  pulse.     The  heart  may  ul- 
timately enlarge. 


4.     LEUKEMIA. 

DEFINITION. 

A  progressive,  chronic  and  permanent  disease  of  the 
blood  and  hematopoietic  organs  (marrow,  spleen  and 
lymph  glands)  especially  those  concerned  in  the  genesis 
of  the  white  corpuscles  which  are  found  to  be  enormously 
increased  in  number. 

The  leucocytosis  here  is  permanent  whereas  in  other 
diseases  it  is  more  or  less  transitory. 

VARIETIES. 

(A)  Spleno-medullary    leukemia    ("myelemia"). 

(B)  Lymphatic  leukemia   C'lymphemia"). 

SPLENO-MEDULLARY   LEUKEMIA.     BLOOD   PICTURE. 

1.     Changes  in  the  white  cells.     Tremendous  increase  in 
the  absolute  count.     Average  is  350,000  per  c.mm. 

The  differential  count  is  (according  to  Webster) : 

(a)  Neutrophilic  myelocytes.  These  average  35%  of 
the  total  white  count.  These  cells  are  large 
mononuclear  cells  with  neutrophilic  granules. 
They  appear  in  two  forms: 

1,  Large  myelocyte  of  Cornil.  Has  a  large,  pale 
eccentric  nucleus  which  is  poor  in  chromatin. 
These  cells  are  only  diagnostic  of  this  disease. 

2.  Small  myelocyte.  Is  about  the  size  of  a  nor- 
mal polynuclear  leucocyte,  has  a  centric 
round  nucleus  staining  deeply  with  the  vari- 
ous aniline  dyes. 

Note. — All  gradations  are  seen  between  these 
two  types, 

10 


(b)  Polynuclear  neutrophile  leucocytes.  These  are 
"relatively"  decreased  in  number.  The  absolute 
count  is  increased.  60,000  to  75,000  of  these 
cells  may  be  present.  They  average  46%  of  the 
total  white  count. 

These  cells  vary  greatly  in  size:    something 
never  seen  in  ordinary  leucocytoses. 

They     are     frequently     degenerated,     their 
nuclei  being  pale  and  showing  karyokinesis, 

(c)  Eosinophiles.  Usually  increased  but  their  per- 
centage relation  to  the  other  white  cells  is  un- 
altered. Average  is  57^.  They  vary  greatly  in 
size. 

(d)  Basophiles.  The  mast  cells  are  increased,  the 
absolute  count  in  some  cases  being  greater  than 
that  of  the  eosinophiles  and  always  proportion- 
ately higher. 

(e)  Lymphocytes.  As  a  rule  the  percentage  is  re- 
duced to  an  average  of  10 '>o.  The  absolute  count 
is  however  increased.  Large  cells  predominate 
over  the  small  cells  and  in  both  forms  degenera- 
tive changes  are  frequent. 

2.  Changes    in   the    red    cells. 

(a)  Oligocythemia.  The  absolute  count  is  decreased 
from  10  to  409c.  The  cells  approach  the  chlo- 
rotlc  type. 

(b)  Nucleated  reds  are  numerous. 

Normoblasts  only. 

If  megaloblasts  and  gigantoblasts  be  present 
the  prognosis  is  bad. 

The  larger  nucleated  red  cells  never  exceed 
the  normoblasts  in  number. 

(c)  Polychromatophilia  is  more  or  less  common. 
Many  cells  show  basophilic  granulations. 

The  following  equations  will  elucidate  the  diagnosis: 

(a)  in  health:        W.B.C.:  R.B.C.: :     7,000:4,500,000 

(b)  inleukemia:    W.B.C.:  R.B.C.: : 350,000: 3,500,000. 

A  ratio  of  1:650  in  the  first  case  as  compared  to 
1:10  in  the  latter. 

3.  Hemoglobin    reduced.     Average  is  40%. 

4.  Color  index  is  low.     Average  is  0.6. 

5.  Low  specific  gravity.     The  blood  is  pale  and  sticky. 

11 


SYMPTOMS   OF   SPLENO-MYELOGENOUS    LEUKEMIA. 

Onset.     General  malaise,  weakness,  pallor,  some  ema- 
ciation and  .digestive  disturbances. 

1.  Progressive  dyspnea  due  to  progressive  increase  in 
size  of  the  spleen. 

2.  Early  enlargement  of  the  spleen.  It  is  usually  pain- 
ful and  progressive. 

3.  Those  symptoms  due  to  splenomegaly  itself. 

(a)  Ascitic  accumulations  in  abdomen. 

(b)  Dropsical  infiltration  of  extremities. 

(c)  Recurrent  hematemesis. 

4.  Hemorrhages  into  the  skin  and  mucous  membranes 
may  follow^  the  appearance  of  the  splenic  tumor. 

Bleeding  from  the  nose  is  very  common. 

A  hemorrhage  or  a  free  diarrhea  may  reduce  the 
size  of  the  spleen. 

The  lymph  glands  may  also  enlarge  after  the  spleen 
has  enlarged  but  not  always. 

Gastro-intestinal  disorders. 

Obstinate  priapism  very  frequent. 

Defective  hearing  and  vision.     (Leukemic  retinitis). 

Febrile  and  afebrile  periods  common. 

The  liver  may  also  become  enlarged. 

LYMPHATIC    LEUKEMIA.      BLOOD    PICTURE. 

1.  An  absolute  leucocytosis  with  a  preponderance  of 
lymphocytes.     Average  leucocyte  count  is  145,000. 

2.  In  contrast  to  the  spleno-myelogenous  form  in  which 
the  granular  cells  are  increased,  we  find  here  an  in- 
crease in  the  nongranular  mononuclear  cells. 

3.  Both  large  and  small  lymphocytes  are  present  depend- 
ing upon  the  stage  of  the  disease. 

4.  These  leucocytes  show  degeneration  of  both  proto- 
plasm and  nuclei  but  only  few  cells  show  mitosis 
which  is  so  common  in  the  other  form  of  leukemia. 

5.  The  lymphocytes  constitute  about  95%  of  the  total 
white  count,  the  polymorphonuclear  cells  therefore 
being  insignificant  in  number. 

6.  Anemia  is  of  a  severer  grade  than  in  the  other  form. 
The  average  hemoglobin  percentage  is  37. 

7.  In  exceedingly  grave  cases  only,  do  we  find  nucleated 
red  cells. 

12 


10 


SYMPTOMS    IN    LYMPHATIC    LEUKEMIA. 

(A)  ACUTE   LYMPHATIC    LEUKEMIA.      (Young  people 
usually  affected.) 

1.  Hemorrhages  into  the  skin. 

2.  Rapidly  developing  cachexia  and  anemia. 

3.  Angina.      (Usually  of  the  ulcerative  type.) 

4.  Swelling   of   the   glands.     Usually   cervical. 

5.  Fever.     103"  to  105\ 

(B)  CHRONIC  LYMPHATIC  LEUKEMIA. 

1.  Occurs  later  in  life. 

2.  Gradual,  progressive  and  painless  enlarge- 
ment of  the  lymph  glands  usually  first  af- 
fecting the  glands  of  the  neck,  then  the 
axillary  and  in  time  become  generalized. 

3.  Spleen  and  liver  may  also  be  enlarged. 

4.  Anemia  approaches  gradually. 

.5.  Hemorrhage  and  fever  are  rare. 

6.  Pruritus  may  be  very  intense. 

7.  Bones  are  very  tender. 

8.  Metabolism  practically  unchanged. 

9.  Small  lymphocytes  predominate. 


5.     HODGKIN'S  DISEASE. 

DEFINITION. 

A    disease    of    the    lymphatic    structures    having    the 
following  characteristics: 

1.  Cervical  glands  enlarged. 

(a)  The  glands  of  the  neck  are  first  to  enlarge 
(sometimes  one  at  the  angle  of  the  jaw.) 

(b)  Only  one  side   at  first  involved. 

(c)  From  this  point  all  the  other  glands  are  in- 
volved progressively  downward,  i.  e.,  axilla,  el- 
bow, groin,  etc. 

Characteristics  of  these  glandular  enlargements: 

(a)  Progressive  increase  in  size. 

(b)  Painless  throughout  the  disease. 

(c)  First  soft,  later  becoming  hard. 

(d)  Discrete:    each    gland    can   be   mapped   out 
from  the  adjacent  gland. 

(e)  Freely  movable  under  the  skin. 

2,  Splenomegaly  not  as  marled  as  in  leukemia. 

13 


3.     Those  features  of  a  secondary  anemia. 

Red  cells  usually  between  3  and  4  million 


But, 


the   more   pronounced   the    cachexia   the   greater   the 
oligocythemia. 

White  ceils  normai  or  perhaps  slightly  increased. 
Average  is  about  10,000. 

Exaggerated  leucocytosis   of  leukemia   is   absent. 
A  relative  lymphocytosis   is   diagnostic. 

May  be  diagnosed  from  spleno-medullary  leu- 
kemia by  the  fact  that  in  Hodgkin's  disease  the  rela- 
tion of  lymphocytes  to  polynuclear  cells  is  3  to  1  in- 
stead of  normal,  1  to  3. 

Those  cases  in  which  the  leucocytes  are  increased 
the  prognosis  is  unfavorable. 

Hemoglobin  reduced  in  proportion  to  R.  B.  C. 

4.     Pressure  symptoms. 

(a)  Dyspnea.  (d)  ,  Ascites. 

(b)  Hydrothorax.     (e)     Swelling  of  extremities. 

(c)  Dysphagia.  (f)      Jaundice. 


DIFFERENTIAL   DIAGNOSIS. 


HODGKIN'S   DISEASE. 


Lymphatic  hyperplasia  is  gen- 
eral but  the  cervical  glands 
are  the  starting  point. 


It  is  first  unilateral  and  sub- 
sequently involves  the  other ' 
side. 

The  glands  grow  rapidly  but 
always  remain  discrete. 


The  glands  are  first  soft  and 
elastic,  later  becoming  hard. 


TUBEKCULAR  CERVICAL  ADENITIS. 

A  localized  disease,  the  cer- 
vical glands  are  more  often 
tubercular  than  any  other 
glands  of  the  body.  It  is 
never  generalized. 

Bilateral  from  the  start  but 
more  marked  on  one  side  than 
on  the  other. 

The  rule  is  that  the  gland- 
ular "kernels"  become  matted 
together. 

At  first  hard  and  the  skin  is 
freely  movable  over  the  ker- 
nels. Later,  the  glands  soften 
and  suppurate.  When  sup- 
puration ensues  the  glands 
become  adherent  to  the  skin, 


14 


DIFFERENTIAL     DIAGNOSIS— Continued. 


HODOKIN'S   DI8EASK. 


Not  only  are  the  lymph  nodes 
affected  but  also  the  spleen. 
Large  nodular  growths  are 
found  in  this  organ,  in  the 
liver,  etc.  This  internal 
lymphatic  hyperplasia  causes 
various  pressure  symptoms: 
ascites,  jaundice,  dyspnea, 
etc.,  according  to  location. 

An  excised  portion  of  a  gland 
shows  lymphoid  structure. 


J  CJiKKCULAK  CKRVICAL  ADEJNITIH 

and   discharging   fistulae   may 
form. 

Lymph    glands    only   affected. 


Tubercle   structure. 


Note — Both  diseases  are  common  in  children  and  in  both 
may  the  tuberculin  reaction  be  obtained.  It  is,  however, 
obtained  only  in  advanced  cases  of  Hodgkin's  disease  when 
the  cachexia  is  very  marked. 


6.     SPLENIC  ANEMIA— BANTI'S  DISEASE. 

DEFINITION. 

A  special  form  of  anemia,  chronic  in  nature,  asso- 
ciated with  enlargement  of  the  spleen  (splenomegaly) 
but  without  palpable  lymphatic  glandular  hyperplasia  and 
by  occurring  by  preference  in  children. 

DIAGNOSIS. 

1.  Tendency  to   hemorrhage,    especially    epistaxis. 

2.  Enlargement  of  the  spleen  associated  with  secondary 
enlargement  of  the  liver  due  to  cirrhosis.  The  texture 
of  the  spleen  is  hard  and  it  increases  with  the  pro- 
gress of  the  disease.  Splenomegaly  is  never  as  great 
as  in  spleno-medullary  leukemia. 

3.  Jaundice  and  pigmentation  of  the  sl<in. 

4.  Blood  picture: 

Very  variable,  though,  in  many  respects,  it  re- 
sembles that  of  secondary  anemia,  i.  e.,  R.  B.  C.  and 
Hb.  reduced  in  same  proportion  and  low  color  index. 
Usually  slight  reduction  in  absolute  W,  B.  C.  Rela- 
tive lymphocytosis  (Webster).  Relative  decrease  in 
polynuclears. 

15 


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7.     SCURVY. 

DEFINITION. 

An  acquired  nutritional  disease  characterized  by  de- 
bility, anemia,  spongy  gums  and  a  tendency  to  hemor- 
rhage, probably  due  to  a  lack  of  vegetables  or  vegetable 
acids   in  the  foods. 

CLASSIFICATION. 

(A)  Scorbutus  or  scurvy. 

(B)  Infantile  scurvy  or  Barlow's  disease. 

DIAGNOSIS   OF  SCORBUTUS. 

1.  ONSET.     Very  insidious.     Early  symptoms  are: 

Progressive  loss  in  weight. 
Weakness  and  pallor. 

2.  CHANGES   IN   THE    MOUTH. 

(a)  Gums  swollen,  bleed  easily,  tend  to  ulcerate,  very 
painful.  In  severe  cases  the  gums  present  a 
fungous  appearance. 

(b)  Teeth  loosened  and  may  fall  out. 

(c)  Fetor  oris,  salivation  and  stomatitis. 

3.  HEMORRHAGES. 

(a)  Mucous  membranes.  Especially  in  mouth  but 
not  as  frequent  as  from  other  places.  Epistaxis 
is  very  frequent. 

(b)  Subcutaneous.    Usually  petechial  in  form. 

Most  commonly  on  lower  extremities. 

After  the  lower  extremities  are  involved  then 
the  arms  and  trunk  become  involved. 

The  hemorrhages  take  place  more  frequently 
in  and  about  the  hair  follicles. 

Deeply  situated  hematoma  may  occur  and 
then  may  ulcerate  through  the  skin. 

(c)  Subperiosteal.     Irregular  nodes  are  formed. 

These  may  also  ulcerate  and  break  through 
the   skin. 

(d)  Arthritic.     Hemorrhage  into  the  joints. 

4.  CACHEXIA    AND   ASTHENIA. 

Palpitation,  feeble  and  irregular  pulse. 

Skin  also  becomes  dry. 

Severe  secondary  anemia.     No  abnormal  cells. 

17 


5.  Rheumatoid  arthritic  pains. 

Knees  and  ankles  most  often  affected. 
Edema  around  ankles  very  common. 

6.  Advanced  cases  may  show: 

Bone  necrosis  and  in  young  persons  separation  of 
the  epiphysis. 

Necrosis  of  the  jaw  is  not  common. 

7.'    SCURVY  SCLEROSIS  oftenest  seen  in  the  legs. 

It  is  an  infiltration  of  the  subcutaneous  tissues 
and  muscles  forming  a  brawny  induration.  The  over- 
lying skin  may  be  blood  stained. 

DIAGNOSIS    OF     INFANTILE     SCURVY     (BARLOW'S     DIS- 
EASE). 

1.  Subperiosteal  hemorrhages  in  the  child's  lower  ex- 
tremities occur  first.  The  child  lies  motionless  and 
its  feet  are  kept  drawn  up  in  flexion. 

These  subperiosteal  hemorrhages  appear  as  ill- 
defined  swellings. 

They  are  not  necessarily  symmetrical. 

Usually  located  around  the  shafts  of  long  bones 
beginning  above  the  epiphyseal  junctions. 

The  bulk  of  the  limb  increases  gradually  and 
visibly. 

2.  Pseudo-paralysis.  As  the  swelling  progresses  the 
lower  limbs  change  from  the  original  position  of 
flexion  to  one  of  extension  and  eversion  and  the  limb 
lies  motionless  and  flaccid.  V/eakness  of  the  back 
follows  shortly  after. 

3.  Swelling  of  one  or  both  scapulas  may  then  appear. 

4.  Swellings  in  upper  extremities  are  next  to  appear. 

They  are  not  as  extensive  as  in  the  lower. 

Usually  seen  about  the  wrists  and  in  the  neigh- 
borhood of  the  epiphysis  of  the  humerus. 
Usually  symmetrical. 

5.  Crepitus.  May  be  elicited  in  several  cases  at  the  junc- 
tion of  the  epiphysis  with  the  daiphysis. 

Usual   places   are:     upper  and  lower   ends   of  fe- 
mur;  upper  end  of  tibia. 

6.  Chest  now  begins  to  sink  "en  bloc." 

18 


7.  Periosteal  thickenings  may  now  appear  on  the  skull 
and  hones  of  the  face. 

8.  Eye  symptoms. 

Proptosis  of  one  eyehall  with  pufRness  and  stain- 
ing of  upper  lid. 

Within  a  few  days  the  other  eye  may  show  the 
same. 

9.  Profound  anemia  in  proportion  to  the  intensity  of  the 
involvement  of  the  limbs. 

10.  Emaciation  is  not  marked  but  asthenia  is  pronounced. 

11.  Fever.     Usually  101°   to  102°  but  very  erratic. 

12.  Teeth.  If  the  teeth  have  appeared,  the  gums  may  be 
spongy. 

(Tiie  essential  lesion  is  subperiosteal  blood  extra- 
vasation which  causes  thickening  and  tenderness  in 
the  shafts  of  the  long  bones.) 

13.  The  disease  usually  follows  the  prolonged  use  of  pro- 
prietary foods  especially  malted  and  condensed  milk 
but  may  also   develop  in  the  breast-fed. 


8.     HEMOPHILIA. 

DEFINITION. 

A  hereditary  and  constitutional  disease  characterized 
by  a  marked  tendency  to  uncontrollable  hemorrhage  oc- 
curring spontaneously. 

A  very  insignificant  injury  may  cause  a  severe  hemor- 
rhage. 

DIAGNOSIS. 

1.  By  the  history  of  "bleeders"  in  the  family.  The  un- 
affected female  is  the  conductor  of  the  disease.  In- 
herited tendency  of  the  male  to  bleed. 

2.  EPISTAXIS  is  the  usual  form  of  bleeding  in  50%. 

Next  in  frequency  is  hemorrhage  from  the  mouth 
and  bowels. 

Hematoma  may  form  under  the  skin. 

Hemorrhages  into  the  joints,  especially  the  knee 
cause  painful  anemic  swellings  which  are  liable  to 
result  in  deformities  and  ankylosis.  They  are  very 
apt  to  be  mistaken  for  tubercular  arthritis.  These 
bloody  effusions  develop  with  remarkable  rapidity. 

19 


3.  The  first  hemorrhage  occurs  before  the  second  year. 

The  early  signs  in  children  may  be:  umbilical 
hemorrhage;  marked  bleeding  during  ritual  circum- 
cision; bleeding  during  teething;  menorrhagia  in  older 
children. 

4.  Coagulation  of  blood  delayed. 

5.  The  blood  shows  no  typical  changes  other  than  that 
seen  in  secondary  anemia  due  to  hemorrhage). 

6.  "No  solitary  hemorrhage,  however  inexplicable,  should 
be  regarded  as  hemophilia;  it  is  necessary  to  show 
that  the  individual  has  been  repeatedly  attacked,  if 
not  from  birth,  from  infancy."     (Bulloch  &  Fildes.) 


9.     PURPURA. 

DEFINITION. 

A  symptom  denoting  hemorrhagic  extravasation  into 
the  skin  and  not  caused  by  traumatism. 

CLASSIFICATION. 

Petechia.    Are  pin-point  hemorrhagic  spots. 
Ecchymoses.     Are  large  spots  resembling  bruises. 

COLOR. 

All  eruptions  vary  in  color  according  to  age  of  the 
purpuric  eruption. 

In  the  beginning  they  are  bright  red  or  scarlet. 

Before  disappearing,  they  pass  through  the  various 
colors  as  seen  after  ordinary  bruises,  becoming  blue- 
black,   greenish-black  or  brownish. 

Purpuric  eruptions  cannot  be  made  to  disappear  on 
pressure. 

With  the  absorption  of  the  effused  blood  and  the  hema- 
tin,  no  trace  remains  to  mark  the  site  of  the  extravasation. 

In  some  forms  of  purpura  the  coagulation  time  is  re- 
tarded. 

CLINICAL  CLASSIFICATION    (Osier). 

1.     SYMPTOMATIC  PURPURA. 

(a)  Infectious. 

(b)  Toxic. 

(c)  Cachectic. 

(d)  Neurotic. 

(e)  Mechanical. 

20 


2.  ARTHRITIC    PURPURA. 

(a)     Purpura  simplex. 

fe)     Schonlein's   disease    (peliosis  rheumatica). 

3.  PURPURA      HEMORRHAGICA      (Morbus      maculosis 

Werlhof). 

1.     SYMPTOMATIC    PURPURA. 

Typhus  and  cerebro-spinal  fevers  are  commonly 
known  as  "spotted  fever"  by  virtue  of  the  petechial  rashes 
so  commonly  found  in  these  affections.  Those  cases  here- 
tofore called  Brill's  disease  are  now  recognized  as  being 
only  typhus  in  a  mild  form.  Plots  has  succeeded  in 
isolating  an  organism  (typhi-exanthematici)  in  typhus 
fever. 

Embolic  processes  into  the  skin  from  pyemia,  septi- 
cemia or  ulcerative  endocarditis  also  give  rise  to  petechia. 
In  the  last  named  condition,  ecchymoses  may  also  be  very 
marked. 

T.ess  commonly,  these  rashes  occur  in  small-pox,  meas- 
les and  scarlet  fever— the  so-called  hemorrhagic  or  "black" 
forms  of  contagious  diseases  which  are  very  dangerous. 
These  petechial  eruptions  and  ecchymoses  occur  in  addi- 
tion to  the  characteristic  rashes  and  are  associated  with 
bleeding  elsewhere. 

Under  the  toxic  variety,  we  include  snake  venom, 
copaiba,  quinine,  belladonna,  mercury,  ergot,  iodides,  ben- 
zol poisoning  in  workers  on  rubber  tires,  etc. 

The  cachectic  variety  is  the  most  common  variety  and 
is  found  in  the  cachectic  states  of  cancer,  tuberculosis, 
Bright's  disease  and  in  old  age.  The  spots  are  in  these 
cases  usually  confined  to  the  extremities. 

It  may  also  occur  in  connection  with  organic  diseases 
of  the  nervous  system:  tabes,  myelitis  and  also  in  hys- 
teria. 

As  a  mechanical  symptom  it  may  be  present  in  w^hoop- 
ing  cough,  epilepsy  and  in  venous  stasis. 

2.     ARTHRITIC   PURPURA. 

(a)      PURPURA   SIMPLEX. 

It  is  the  mildest  form  and  occurs  most  com- 
monly in  children. 

Crops  of  petechial  spots  appear  on  the  legs, 
especially  on  the  flexor  aspect  and  less  com- 
monly on  the  trunk  and  arms. 

21 


Joint  symptoms  are  not  severe. 

Diarrhea  usually  present  but  no  fever. 
Recovery  in  from  7  to  10  days. 

(b)      PURPURA       (PELIOSIS)       R  H  E  U  M  A  T  I  C  A 
(SCH5NLEIN'S  DISEASE). 

Multiple  arthritis. 

Many  kinds  of  eruptions: 

Usually  urticaria  and   erythema   exuda- 
tivum. 

Sometimes  purpuric. 
Often  purpura  and  urticaria. 
Rashes  first  appear  on  affected  joints  or  on 
legs. 

Males  usually  affected  (20  to  30  years  of 
age). 

Articular  pains  are  severe,  especially  when 
the  rashes  come  out. 

Fever:    101°  to  103°. 

Sore  throat  very  common. 

Recovery  is  the  rule  but  the  sore  throat  may 
persist. 

VISCERAL   LESIONS    IN    PURPURA. 

May  occur  in  any  form  of  purpura. 

(a)  Gastro-intestinal  crises  of  pain,  vomiting,  melaena 
and  diarrhea  so  that  an  attack  may  be  mistaken 
for  appendicitis  or  intussusception.  Purpura  as- 
sociated with  colic  is   called    Henoch's   purpura. 

(b)  Splenomegaly  usually  present  in  these  cases. 

(c)  Albuminuria  and  acute  nephritis  may  occur  and 
be  the  most  serious  symptoms. 

PURPURA  HEMORRHAGICA.   (MORBUS  MACULOSIS 
OF  WERLHOF). 

1.  Includes  all  cases  of  purpura  associated  with  hem- 
orrhages from  the  mucous  membranes. 

2.  Usually   occurs   in   young   and    delicate    girls    but 
adults  may  also  be  attacked. 

3.  Prodromes.     For  a  few  days  there  may  be  weak- 
ness. 

4.  Onset.     Purpuric  spots  on  the  skin  which  rapidly 
increase  in  size  and  in  number. 

22 


5.  Hemorrhages  from  any  mucous  membrane  in  the 
body. 

Usual  forms  are  epistaxis,  hematuria  and 
hemoptysis.  Hemorrhages  cause  a  severe  anemia 
and  may  prove  fatal. 

6.  Fever.     Usually  present  but  slight. 

7.  Favorable  cases  recover  after  10  to  14  days. 

8.  Purpura   fulminans.     Death   may  occur   within   24 
hours. 

This  usually  occurs  in  children. 
Hemorrhages  are  usually  cutaneous. 
Death  occurs  even  before  hemorrhages  occur 
from  the  mucous  membranes. 


10.     BLOOD  POISONING. 

Sapremia  and  Septicemia. 

DEFINITION. 

Blood  poisoning  is  an  indefinite  term  and  is  not  ac- 
cepted as  a  cause  of  death.  It  is  best  described  under 
the  headings  of  sapremia  and  septicemia. 

1.  SAPREMIA.  Such  an  infection  as  occurs  after  the  re- 
tention of  blood  clots  or  fragments  of  membranes  in 
the  uterus  after  labor  or  abortion.  The  bacteria  thrive 
on  this  decomposed  materia!  in  the  womb. 

2.  SEPTICEMIA.     This  is  further  subdivided  into: 

(A)  Toxemia  or  septic  intoxication.  In  which 
toxins  alone  are  absorbed  from  the  focus  of 
growing  pathogenic  or  pyogenic  bacteria  in 
the  living  tissues. 

(B)  Progressive  septicemia  or  bacteremia.  This 
occurs  when  bacteria  enter  the  circulation. 

PYEMIA.  Signifies  secondary  multiple 
metastatic  abscesses  in  the  tissues  dur- 
ing the  course  of  septicemia. 

DIAGNOSIS  OF   SAPREMIA. 

The  saphrophytic  bacteria  acting  upon  the  dead  ma- 
terial in  the  womb,  produces  toxins  which  are  discharged 
into  the  circulation  with  the  following  results: 
1.     Intense  chills,  high  fever  and  rapid  pulse. 

23 


2.  Flushed  skin  and  dry  coated  tongue. 

3.  Change  in  lochia  and  tenderness  over  uterus. 

4.  By  proper  cleansing  of  the  womb  of  the  decomposed 
material  all  symptoms  abate. 

5.  Usually  occurs  2  to  3  days  post-partum, 

DIAGNOSIS  OF  SEPTICEMIA  AND   PYEMIA. 

1.  Fever,  chills  and  sweats. 

Fever  is  remittent  in  character.  Highest  in 
pyemia  and  in  this  form  distinctly  "septic"  in  char- 
acter. 

Chills  that  precede  or  accompany  the  elevation  of 
temperature  are  quite  severe. 

The  fever  occurs  in  paroxysms  but  not  with  the 
same  regularity  as  in  malarial  fevers. 

The  fever  in  septicemia  is  much  lower  than  in 
sapremia  and  yet  the  patient  feels  worse. 

The  orderly  sequence  of  chill,  fever  and  sweat 
is  not  as  characteristic  as  in  malaria. 

Diaphoresis  is  most  marked  in  pyemia. 

2.  Enlarged  and  painful   spleen. 

3.  Septic  diarrlnea   and   vomiting. 

4.  Septic  arthritis  is  pathognomonic  of  pyemia.  It  is 
usually  associated  with  skin  eruptions,  the  most  fre- 
quent being  petechia. 

5.  Septic    endocarditis   is   a   very   common   complication. 

6.  Septic  nephritis  may  occur  in  pyemia. 

Even  when  nephritis  does  not  occur  the  urine  al- 
ways contains  albumin. 

7.  Intense  nervous  manifestations.  There  may  be  de- 
lirium, prostration  and  coma.  Many  pass  into  the 
so-called  "typhoid  state." 

8.  Metastatic  abscesses  as  above  described  (in  the  skin, 
kidney,  joints,  endocardium)  are  diagnosed  by  an  in- 
crease in  the  severity  of  the  symptoms  and  signify 
pyemia. 

9.  Blood.  Marked  leucocytosis  with  an  increase  in  per- 
centage of  polynuclear  cells. 

Blood  cultures  taken  directly  from  a  vein  may 
show  staphylococci,  streptococci,  colon,  gonococci  or 
pneumococci.  Repeated  cultures  should  be  made  if 
the  first  be  negative. 

24 


11.     ERYTHREMIA. 
Vaquez'   Disease — Polycythemia  Vera. 

DEFINITION. 

A  persistent  increase  in  the  R.  B.  C.  associated  with 
plethora,  splenomegaly  and  at  times  cyanosis.  It  is  a 
disease  of  the  bone  marrow  (of  the  erythroblastic  tissues 
as  compared  to  the  leucoblastic  tissues  in  leukemia. 

Hyperglobulism  in  consequence  to  high  altitudes  is 
not  included  under  this   head. 

DIAGNOSIS. 

1.  FACIAL  APPEARANCE. 

Superficial  blood  vessels,  capillaries  and  veins 
look  full.  Skin  is  therefore  congested.  In  warm 
weather  the  face  is  brick-red  in  color.  In  cold,  it  is 
cyanosed. 

2.  SPLENOMEGALY  not  as  great  as  in  leukemia. 

The  enlargement  is  hard,  firm  and  painless  and 
may  vary  in  size  from  time  to  time.  It  may  cause 
ascites. 

3.  HYPERGLOBULISM. 

The  corpuscular  volume  greatly  exceeds  that  of 
the  plasma. 

The  polycythemia  ranges  from  7  to  12  million 
R.  B.  C.  per  c.mm. 

Red  cells  are  usually  normal  in  size  and  shape. 
A  few  nucleated  reds  may  be  present. 

Hemoglobin  ranges  from  130  to  160%. 

Color  index  relatively  low. 

Specific  gravity  is  high. 

Moderate  leucocytosis  without  any  change  in  the 

differential  count. 

4.  Headache,   flushing,   giddiness. 
Constipation. 
Albuminuria. 

High  blood  pressure. 


25 


CHAPTER  II. 

THE  BLOOD. 

DEFINITION. 

A  fluid  tissue  circulating  in  closed  vascular  channels 
regulated  by  the  activity  of  the  heart  and  having  certain 
well  defined  functions: 

(a)  Nutrition.     (Maintaining  life). 

(b)  Excretion  of  v^aste  matter  via  skin  and  kidneys. 

(c)  Regulation  of  body  temperature. 

(d)  Respiration.     Its  hemoglobin  content  forming  loose 
combinations  with  oxygen  and  carbon  dioxide. 

(e)  Distribution  of  internal  secretions. 

COLOR.    Due  to  a  ferruginous  substance:    hemoglobin  (Hb.) : 

Arterial  blood  is  a  bright  scarlet  color. 

Venous  blood  is  a  purplish  blue. 

Bright  cherry-red  color  occurs  in  certain  forms  of 
poisoning  especially  carbolic  acid. 

Brownish-red  or  chocolate  color  occurs  in  poisoning 
with  chlorate  of  potash  and  aniline. 

Whitish-red  or  milky  colored  blood  occurs  in  leukemia. 

Pale  and  watery  blood  is  seen  in  hydremia  and  in 
chlorosis. 

REACTION.    Alkaline  to  special  indicators. 

A  lowered  alkalinity  occurs  in  diabetes  and  is  a 
very  bad  prognostic  sign.  During  diabetic  coma,  the  re- 
action may  even  be  acid. 

COMPOSITION. 

Plasma — 50%   of  the  volume  of  the  blood. 
Formed   elements  floating  in  the  plasma — 50%. 

Relation  of  Volume  of  Cells  to  Plasma: 

By  means  of  Daland's  hematocrit  which  consists  of 
2  calibrated  tubes,  the  divisions  of  which  are  100  equal 
portions,  each  division  approximating  100,000  cells,  the 
blood  is  centrifuged  and  the  plasma  becomes   separated 

26 


from  the  morphological  elements.  It  gives  us,  therefore, 
a  rough  blood  count.  If  the  cellular  portion  stops  at 
point  50  on  the  tube  it  means  a  red  count  of  5  million. 
(50x100,000.) 

VOLUME    INDEX. 

With  Daland's  hematocrit  point  50  represents  the  nor- 
mal, because  the  volume  of  the  plasma  equals  the  volume 
of  corpuscles. 

Supposing  the   cellular   portion   stopped   at   point   40. 

40 

The  volume  per  cent,  would  be  t^=^  80%. 

Label  this  volume  percentage  "A."  It  is  to  be  the 
numerator  in  the  determination  of  volume  index. 

Now  count  the  number  of  R.  B.  C.  (see  page  37). 
Suppose  we  counted  4,500,000.  Since  the  normal  red  count 
is  taken  at  5,000,000,  we  must,  in  order  to  get  the  per- 
centage proceed  as  follows: 

Label     this     percentage 


4,500,000  ^  45  _  9 
5,000,000       50       10  ~ 


"B."     It   is   to   be   the    de- 
nominator. 

The  volume  index  is  therefore  the  quotient  of  the 
volume  per  cent.  (A)  as  obtained  by  the  hematocrit  and 
the  actual  blood  count  per  cent.  (B).  Thus,  in  the  above 
instance: 

A      Hematocrit  volume  of  red  cells  in  '/o       f  Volume     in- 

— = =  -'  dex    of    red 

B       Percentage  counted  red  blood  cells       [  cells. 

Then  inserting  figures:      ^^^  =-t~-     Normally  it  is  1. 

90%        9 

According  to  Capps,  this  volume  index  is  constantly 
increased  in  pernicious  anemia.  The  color  index  never 
exceeds  the  volume  index.  In  primary  and  secondary 
anemias  this  factor  is  decreased  and  oftentimes  the  color 
index  falls  below  the  volume  index.  Color  index  is  de- 
scribed on  page  38. 

COMPOSITION   OF    BLOOD    PLASMA. 

Plasma  is  the  liquid  portion  of  the  circulating  blood. 
When  blood  clots  (see  page  52)  the  liquid  which  exudes 
from  the  clot  is  called  serum. 

Serum   consists  of: 

Proteids:    serum   albumin  and   serum  globulin. 
Glucose,    extractives,    calcium   salts,    sodium    and    po- 
tassium chlorides,  carbonates,  phosphates,  etc, 

27 


The    chief   extractives   are: 

Fat,  sugar,  urea,  uric  acid,  sarco-lactic  acid, 
lecithin,  cholesterin,  glycuronic  acid,  creatin,  car- 
bamic  acid,   glycogen,  hippuric  acid. 

THE  MORPHOLOGICAL  OR  FORMED  ELEMENTS  OF  THE 
BLOOD. 

fRed  cells   (R.  B.  C). 
}  White  cells   (W.  B.  C). 
(  Blood  plates. 

ENZYMES  in  the  blood. 
'  Glycolytic   ferment. 

Lipolytic  ferment.     (Fat  synthetizing.)    . 

Oxidases. 
-{  Proteolytic   properties   of   leucocytes. 

Internal  secretions  as  adrenalin,  etc. 

Amboceptors. 
^  Complements. 

GASES  of  the  blood. 
f  Oxygen. 
\  Carbon  dioxide. 
(  Nitrogen. 

Arterial   blood.  Venous   blood. 

Oxygen 21.6% 6.8% 

Carbon  dioxide 40.3% 48.0% 


BLOOD  PRESSURE. 

NORMAL  FIGURES.     (Janeway's). 

Infants 75  to    90  mm.  Hg.  "] 

Children  over  2  years.  ...   90  to  110  mm.  Hg.   !     Maximum 

Young  adults 110  to  130  mm.  Hg.   {       systolic 

Older  adults 110  to  145  mm.  Hg.  j 

HOW  TO  OBTAIN    NORMAL   B.  P. 

Consider  a  person  aged  20  as  having  a  B.  P.  of  120. 
for  every  2  years  above  this  age  add  1  mm.  Hg. 
Hence:  — 

At  40,  the  B.  P.  would  be  130  mm.  Hg. 
At  50,  the  B.  P.  would  be  135  mm.  Hg. 

Permissible  variations  which  occur  normally. 

Seventeen  mm.  Hg.  above  or  below  would  be  the  nor- 
mal figure  for  any  given  age. 

28 


THE  SPHYGMOMANOMETER  IN  LIFE  INSURANCE. 

1.  In  those  applicants  who  are  overweight  the  blood 
pressure  tests  determine  whether  the  company  should 
take  the  risk. 

2.  It  is  a  recognized  fact  that  permanent  changes  in  the 
kidney  cannot  exist  without  causing  an  increase  in 
the  B.  P.  So  that,  if  an  applicant  does  show  a  faint 
trace  of  albumin  and  casts  are  present  in  scanty 
numbers,  this  evidence  alone  will  not  cause  an  ab- 
solute rejection  unless  his  B.  P.  is  decidedly  increased. 

3.  Signs  of  beginning  pathological  change  in  the  cardio- 
vascular-renal system  can  be  recognized  by  this  in- 
strument long  before  we  can  demonstrate  any  ab- 
normal findings  in  the  heart,  pulse  or  urine. 

4.  A  blood  pressure  exceeding  145  in  a  person  before 
middle  life,  or  a  reading  of  160  after  middle  life  has 
passed  must  be  considered  as  abnormal.     (Janeway). 

TO   OBTAIN   THE    MAXIMUM    SYSTOLIC    B.   P. 

To  obtain  the  maximum  systolic  blood-pressure  a 
broad  arm  piece  should  be  used.  When  the  pulse  at  the 
wrist  is  obliterated  the  height  of  the  mercury  column  is 
equivalent  to  the  maximum  systolic  pressure.  Many  ob- 
servers claim  that  it  is  better  to  accept  the  reappearance 
of  the  radial  pulse  after  obliteration  than  the  initial  dis- 
appearance of  the  radial  pulse.  The  Janeway  apparatus 
and  the  Tycos'  sphygmomanometer  are  best  recommended. 
The  minimum  diastolic  blood-pressure  is  obtained  by  let- 
ting the  pressure  fall  5  mm.  Hg.  at  a  time  and  at  the  same 
time  watching  the  amplitude  of  the  pulsations  of  the  mer- 
cury column  or  oscillations  of  the  needle — and  at  that  point 
where  the  greatest  amplitude  occurs,  that  point  registers 
the   diastolic   blood-pressure. 

The  auscultatory  method  may  also  be  employed. 


HYPOTENSION. 

Definition:  A  blood  pres- 
sure reading  that  is  lower 
than  what  it  should  be  at  any 
given  age  and  under  ordinary 
conditions. 

In  recent  years  hypotension 
has  come  to  be  looked  upon  as 
both  a  diagnostic  and  a  prog- 
nostic factor.    If  one  will  only 


HYPERTENSION. 

Definition:  A  very  notice- 
able increase  in  blood  pres- 
sure above  the  average  for 
any  given  age.  It  may  reach 
the  300  mark  and  it  may  be 
temporary  or  permanent.  It 
is  only  a  symptom  and  it  is 
our  duty  to  investigate  the 
cause.     It  is  also  well  to  re- 


29 


HYPOTENSION. 

bear  in  mind  that  whenever 
vaso-dilatation  occurs  in  con- 
sequence to  a  vaso-motor 
paresis,  the  blood  vessels  be- 
come excessively  dilated  and 
consequently  the  blood  pres- 
sure falls,  it  will  be  very  easy 
to  interpret  the  meaning. 
Such  a  vaso-motor  paresis  is 
the  cardinal  factor  in  shock 
and  collapse.  In  these  condi- 
tions the  greater  the  fall  in 
blood  pressure  the  more  dan- 
gerous does  the  patient's  con- 
dition become. 

Hypotension  is  a  recent  ad- 
ditional diagnostic  point  in 
typhoid  fever.  In  fact,  of  all 
the  acute  infections  which 
may  be  accompanied  by  a  low 
pressure,  typhoid  ranks  first 
and  pneumonia  second.  It  has 
also  been  noticed  here  that 
the  hypotension  bears  a  rela- 
tion to  the  toxic  symptoms. 
As  the  intoxication  increases 
(provided  certain  complica- 
tions are  absent)  the  blood 
pressure  falls  (vaso-motor 
paresis).  On  the  other  hand 
with  the  advent  of  a  compli- 
cation like  a  perforative  peri- 
tonitis the  blood  pressure  will 
rise.  Then,  again,  the  blood 
pressure  reading  will  easily 
differentiate  between  a  hem- 
orrhage of  the  bowel  and  a 
perforation  followed  by  peri- 
tonitis. Intestinal  hemor- 
rhage is  always  accompanied 
by  a  low  blood  pressure, 
whereas  perforative  peritoni- 
tis causes  an  elevation  of 
blood  pressure. 


HYPERTENSION. 

member  that  it  is  often  a  salu- 
tary and  beneficent  condition 
not  to  be  interfered  with. 

A  patient  whose  arterial 
tension  exceeds  260  mm.  Hg. 
is  liable  to  die  suddenly. 

The  usual  causes  of  hyper- 
tension are  found  resident 
either  in  the  cardio-vascular 
system  or  in  the  kidneys.  A 
good  vv^orking  rule  is  as  fol- 
lows: A  permanent  increase 
in  blood  pressure  in  a  young 
adult  or  in  one  in  early  mid- 
dle life,  in  the  absence  of  or- 
ganic changes  in  the  heart, 
blood  vessels  or  kidneys, 
must  be  explained  by  the 
presence  of  a  chronic  toxemia, 
or  a  poisoning  arising  from 
some  error  in  metabolism, 
either  intestinal,  urinary  or 
both.  With  the  advancement 
in  years  the  blood  pressure 
naturally  increases  progres- 
sively. 

The  Sphygmomanometer 
also  has  its  uses  in  obstetrics. 
It  has  been  employed  to  de- 
tect the  development  of  the 
toxemias  of  pregnancy  and 
nephritis  occurring  in  those 
conditions.  After  exhaustive 
clinical  study,  we  must  con- 
clude that  the  taking  of  blood 
pressure  readings  is  just  as 
important  as  the  repeated 
urinary  examinations  and 
pelvimetry  in  pregnancy.  In 
these  cases,  where  hyperten- 
sion is  found,  we  can  explain 
its  presence  by  a  toxemia  by 
virtue  of  the  metabolic  waste 
products  being  absorbed  in 
the  system.     As  far  as  it  is 


30 


HYPOTENSION. 

In  passing  it  may  be  stated 
that  Barach  has  found  the 
blood  pressure  in  enteric  fever 
usually  below  the  century 
mark,  and  it  does  not  bear 
any  relation  to  the  pulse  rate 
nor  the  temperature. 

Before  dismissing  the  sub- 
ject of  hemorrhage,  it  is  well 
to  remember  that  with  the 
exception  of  cerebral  hemor- 
rhage, all  other  hemorrhages 
(either  visible  or  concealed) 
must  be  accompanied  by  a 
lowering  in  pressure.  The 
lowering  is  in  direct  propor- 
tion to  the  quantity  of  blood 
lost'.  However,  in  favorable 
cases  where  regeneration  of 
the  blood  takes  place,  the  vol- 
ume of  the  blood  (its  watery 
constituent)  is  soon  restored 
almost  to  normal,  the  hypo- 
tension is  only  short  lived.  It 
is,  therefore,  a  valuable  prog- 
nostic as  well  as  diagnostic 
feature. 

Returning  to  pneumonia,  we 
may  state  that  we  are  also 
dealing  with  an  intoxication 
which  may  cause  vascular 
paresis.  The  best  way  to  de- 
tect such  a  failure  in  the  cir- 
culation is  by  daily  and  fre- 
quent blood  pressure  readings. 
Circulatory  depression  in  con- 
sequence of  such  a  toxemia  is 
always  accompanied  by  a  fall 
in  blood  pressure,  whereas  it 
has  been  noted  that  typhoid 
bears  no  relation  between  the 
pulse  rate  and  the  blood  pres- 
sure, we  do  find  in  pneu- 
monia such  a  correlation.  Ac- 
cording to  Gibson,  the  situa- 


HYPERTENSION. 

possible  to  lay  down  rules  in 
these  cases,  we  may  say  that 
a  blood  pressure  below  125 
could  be  disregarded;  a  pres- 
sure from  125  to  150  needs 
careful  watching  and  moder- 
ate eliminative  treatment; 
and  that  a  pressure  over  150 
needs  very  active  eliminative 
treatment  and  will,  in  all 
probability,  especially  if  it 
shows  a  tendency  to  climb 
higher,  require  the  induction 
of  premature  labor. 

In  concluding  the  subject 
of  hypertension,  the  diag- 
nostic value  of  this  phenome- 
non can  readily  be  seen  in 
cases  of  cerebral  hemorrhage. 
This  increased  blood  pressure 
is  the  most  reliable  and  diag- 
nostic sign.  It  is  readily  dif- 
ferentiated from  cerebral  em- 
bolism by  the  fact  that  this 
latter  condition  is  accom- 
panied by  a  low  pressure. 
The  elevation  of  the  blood 
pressure  in  cerebral  hemor- 
rhage bears  a  direct  relation 
to  the  increase  in  intra-cra- 
nial  tension  so  that  in  cases 
where  the  hemorrhage  in- 
creases in  size  the  pressure 
increases  in  proportion.  On 
the  other  hand,  if  the  cranial 
encroachment  is  a  slow  and 
chronic  process  like  a  tumor 
there  is  no  effect  upon  the 
blood  pressure.  Finally,  as 
before  stated,  cerebral  hem- 
orrhage is  the  only  hemor- 
rhage which  is  accompanied 
by  hypertension;  all  other 
forms  of  hemorrhage  are  ac- 
companied by  a  diminution  in 
blood  pressure. 


HYPOTENSION. 

tion  in  pneumonia  may  be 
summed  up  as  follows: 
"When  arterial  pressure  ex- 
pressed in  millimeters  of  mer- 
cury does  not  fall  below  the 
pulse  rate  expressed  in  beats 
per  minute,  this  fact  may  be 
taken  as  excellent  augury, 
while  the  converse  is  equally 
true." 

Although  a  high  blood  pres- 
sure is  invariably  associated 
with  aortic  regurgitation,  it  is 
only  valvular  disease  which 
has  hypertension  as  a  diag- 
nostic feature.  In  all  the 
other  valvular  lesions,  as  well 
as  all  organic  lesions  of  the 
heart,  we  find  hypotension. 

Emerson's  findings  in  tu- 
berculosis of  the  lungs  is  as 
follows:  Hypotension  in  pul- 
monary tuberculosis  is  (1)  a 
very  marked  and  constant  fac- 
tor in  advanced  cases;  (2) 
present  but  not  so  very  mark- 
ed in  moderately  advanced 
cases;  (3)  and  it  can  often- 
times be  demonstrated  in  the 
incipient  stage,  and  even  be- 
fore the  development  of  physi- 
cal signs.  Therefore,  it  may 
be  inferred  that  the  longer 
the  disease  has  existed  the 
more  marked  will  the  lower- 
ing in  blood  pressure  be.  He 
also  claims  that  in  those  cases 
where  the  trend  is  towards  re- 
covery we  will  note  a  progres- 
sive return  to  a  normal  pres- 
sure. 

We  are  very  frequently  call- 
ed upon  to  differentiate  the 
various  forms  of  coma  and  the 


32 


HYPOTENSION. 

task  is  not  always  very  easy. 
Edgecombe  has  remarked  the 
noticeable  frequency  of  hypo- 
tension in  epileptic  coma  in 
contrast  to  hypertension 
which  accompanies  uremia. 

In  conclusion,  it  is  well  to 
add  that  wherever  life  is  low 
as  in  cachectic  states,  the 
blood  pressure  tends  to  fall 
progressively. 

SPECIFIC  GRAVITY.     Varies  from  1.050  to  1.062. 
In  children  it  is   nearer  to   1.050. 
The  average  is  1.055. 

According  to  Schmaltz,  the  sp.  gr.  is  in  direct  rela- 
tion to  the  amount  of  hemoglobin  and  the  volume  of  the 
red  cells  (excepting  in  nephritis,  circulatory  disturbances, 
leukemia,  post-hemorrhagic  anemia  and  inanition.  His 
figures  are: 

With  a  sp.  gr.  of  1.059    Hb.  is  100% 

With  a  sp.  gr.   of  1.0575 Hb.   is     90% 

With  a  sp.  gr.  of  1.056   Hb.  is     S07c 

With  a  sp.  gr.  of  1.0535 Hb.  is     75% 

With  a  sp.  gr.  of  1.052   Hb.   is     70% 

With  a  sp.  gr.  of  1.051   Hb.  is     65% 

With  a  sp.  gr.  of  1.049    Hb.  is     60% 

With  a  sp.  gr.  of  1.048   Hb.  is     55% 

With  a  sp.  gr.  of  1.0455 Hb.  is     50% 

With  a  sp.  gr.  of  1.0425 Hb.  is     45% 

With  a  sp.  gr.  of  1.041   Hb.  is     40% 

With  a  sp.  gr.  of  1.038   Hb.  is     35% 

With  a  sp.  gr.  of  1.035    Hb.  is     30% 

With  a  sp.  gr.  of  1.030    Hb.  is     20% 

Hammerschlag's   Method   of   Determination   of  Sp.   Gr. 

Make  a  mixture  of  chloroform  (sp.  gr.  1.526)  and  ben- 
zol (sp.  gr.  0.889)  so  that  it  is  almost  like  that  of  normal 
blood   (1.050  to  1.062). 

A  drop  of  fresh  blood  from  a  capillary  blood  pipette 
is  allowed  to  fall  into  this  mixture.  It  will  either  sink  or 
rise.  If  it  sinks  to  the  bottom,  add  chloroform  drop  by 
drop;  and  if  it  rises  or  floats  add  benzol  drop  by  drop; 
until  the  drop  of  blood  remains  stationary  in  the  mixture. 
Filter  very  quickly  because  evaporation  will  occur,  and 
read  the  sp.  gr.  by  means  of  a  hydrometer  inserted  into 

the  mixture. 

33 


RED  BLOOD  CORPUSCLES. 
(ERYTHROCYTES.) 

MORPHOLOGY. 

1.  In  mammals,  they  are  flat,  circular,  non-nucleated 
discs,  iy2  microns  or  1/3200  of  an  inch  in  diameter, 
having  a  pale  central  area. 

In  fresh  blood,  the  red  cells  show  a  tendency  to 
"coin-roll"  formation. 

As  fresh  blood  dries  upon  the  slide,  the  red  cells 
become  crenated;  that  is  to  say,  spinous  projections 
from  the  cell  appear  like  a  cogged  rim. 

2,  In  birds,  reptiles,  amphibians,  camels,  they  are  bi- 
convex, oval  and  nucleated.  The  largest  cells  are 
found  in  the  amphiba. 

PATHOLOGICAL   RED   CELLS. 

1.  Pessary   or  ring   cell. 

Large  pale  central  area  with  a  small  rim  of  pro- 
toplasm. They  are  called  "dropsical  cells"  and  are 
very  diagnostic  of  chlorosi^. 

2.  Nucleated  red  cells. 

(A)  Normoblasts.  (Trachyochromatic  erythroblasts) . 
A  matured    normoblast   can  thus  be  recognized: 

Size  and  shape  about  that  of  a  normal  R.  B.  C, 
but  it  has  a  nucleus.  If  a  trifle  smaller  in  size 
it  is  called  a  mlcroblast. 

Both  together  signify  REGENERATION  of 
the  blood  and  are  especially  found  after  hemor- 
rhage. 

Normoblasts  stain  more  intensely. 

Its  nucleus  is  about  one-third  of  its  diameter. 
It  is  densely  stained,  more  homogenous,  sharply 
defined,  spheroid  and  devoid  of  chromatin  net- 
work. It  is  usually  situated  towards  the  peri- 
phery. 

An  immature  normoblast  shows  a  very  dis- 
tinct network,  is  larger  and  lighter  in  color  and 
the  chromatin  fibers  are  radially  arranged  and 
frequently  shows  mitotic  figures.      (Howell.) 

(B)      Megaloblasts.     (Amblyochromatic  erythroblasts). 
Size:    larger  than  normoblasts. 
Protoplasm:     usually  swollen  and  enlarged. 
Hemoglobin:    as  a  rule  in  excess. 

34 


(For  Drawings) 


oO 


Usually  poychromatic,  the  shade  of  the  stain 
varying  from  yellow  to  purple. 

Nucleus:  very  large,  varying  from  6  to  10 
microns  and  may  assume  many  forms.  As  a 
rule  it  is  ill-defined  and  shows  feeble  basic  stain- 
ing properties. 

Megaloblasts  signify  abnormal  DEGENERA- 
TION. 

They  appear  in  leukemia,  pernicious  anemia, 
infection  with  the  Bothriocephalus  Latus,  nitro- 
benzol  poisoning,  severe  anemia,  etc. 

When  the  nucleus  of  a  nucleated  R.  B.  C. 
exceeds  20  microns  it  is  termed  gigantoblast  of 
Ehrlich. 

3.  Poikilocytosis.  The  simultaneous  variation  in  both 
size  and  shape  of  the  red  cells.  It  is  very  character- 
istic of  pernicious  anemia. 

4.  Microcytes  and  macrocytes.  The  normal  sized  R.  B.  C. 
is  also  called  a  normocyte.  If  a  cell  is  a  little  smaller 
it  is  a  microcyte.  If  a  little  larger  than  a  normocyte, 
it  is  a  macrocyte.  These  cells  occur  in  grave  and 
in  pernicious  anemia. 

5.  Polychromatophilia  or  polychpomasia. 

The  normal  red  cells,  when  a  smear  is  fixed  and 
stained,  stains  only  with  acid  dyes.  Hemoglobin  is 
therefore  said  to  be  acidophilic. 

Abnormal  red  cells  not  only  show  affinity  for  acid 
dyes  but  basic  dyes.  These  red  cells  instead  of  ap- 
pearing monochromatic  (one  color)  will  appear  with 
several  colors :    gray,  slaty,  purple,  violet,  etc. 

There  are  two  distinct  forms: 

Polychromatophilic  degeneration  of  Gabritscliew- 
sky.  In  which  there  is  a  diffuse  basophilic  staining 
of  the  cells. 

Polychromasia  of  Maragliano  in  which  the  baso- 
philia is  punctate.  It  is  very  closely  related  to  the 
basophilic  degeneration  of  Grawitz. 

6.  Basophilic  degeneration.  (Grawitz.)  Granules  of  vary- 
ing size  appear  in  the  body  of  the  R.  B.  C.  and  stain 
with  basic  dyes.  Very  diagnostic  of  lead  poisoning. 
It  is  also  common  in  diabetes,  myelogenous  leukemia, 
pernicious  anemia,  severe  secondary  anemias  espe- 
cially those  following  malignant  disease,  eruptive 
fevers  and  malaria. 

36 


7.  Microcyte   is  a   red   cell   smaller   than  a   normal   cell. 
Diameter  varies   from  ZV2   to   6/a. 

8.  Macrocyte    is    a    cell    larger    than    a    red    cell.      Size 
varies  from  9V^  to  12;Ct. 

NUMBER   OF    RED    BLOOD   CELLS. 

Males:        5,000,000  per  c.mm. 

Females:   4,-500,000  per  c.mm. 

Oligocythemia:     Pathological  reduction  in  number.     As  a 

rule  there  is  a  corresponding  decrease  in  Hb. 

It  occurs  in  nearly  all  forms  of  anemia  and  as  a  re- 
sult of  the  toxins  of  specific  fevers. 

Polycythemia      (Polyglobulia):     increase     in     number     of 
R.  B.  C. 

High   altitudes.     50,000   cells   for   every   1000   feet  as- 
cension. 

Watery  diarrheas. 

Severe  diuresis  and  ascites.     Numbers  2  and  3  cause 
increased  concentration  of  the  blood. 

4.  Cardiac  diseases.    All  forms  of  cyanosis. 

5.  Drugs  causing  vaso-constriction. 
Diseases  of  the  adrenal  glands. 

Phosphorus    poisoning    and    acute    yellow    atrophy    of 
the  liver. 
Hepatic  insufficiency. 

COUNTING  THE  NUMBER  OF   R.  B.  C. 

Prick  the  tip  of  finger  or  ear,  and  with  blood  pipette 
No.  101,  draw  blood  up  to  the  0.5  mark. 

Now  draw  enough  Hayem's  solution  up  to  101  mark 
and  shake  vigorously  for  at  least  one  minute.  This  gives 
a  200  dilution. 

Discard  the  first  few  drops  and  then  blow  one  drop 
on  to  the  center  piece  of  the  Thoma-Zeiss  hemocytometer 
and  adjust  the  special  cover-slip  carefully  in  place  until 
Newton's  rings  are  visible. 

Examine  first  with  low  power  lens  to  see  if  the  red 
cells  are  evenly  distributed.    If  not  make  a  new  specimen. 

With  high  power  lens,  begin  at  upper  left-hand  cor- 
ner and  proceed  downward,  being  guided  by  the  ruled 
lines,  then  upward,  then  down  again  and  count  the  num- 
ber  of    R.    B.    C.    in    80    squares.      To    this    factor   add    4 

37 


ciphers.  Providing  the  dilution  is  200,  this  number  repre- 
sents the  number  of  red  cells  per  c.mm.  If  we  counted 
325   cells,   the   count  would   be   3,250,000. 

If  blood  has  been  drawn  past  the  0.5  mark,  for  ex- 
ample 0.6,  proceed  as  follows:  Divide  the  number  of  red 
cells  counted  in  the  80  squares  by  the  division  stopped 
at  and  multiply  by  5000.  Suppose  we  counted  390  cells. 
Dividing  this  by  0.6  w^e  get  650.  Then  650x5000  equals 
3,250,000. 

Owing  to  the  presence  of 
bichloride,  the  fluid  cannot  be 
mixed  with  an  aniline  color- 
ing substance  to  stain  the 
leucocytes,  and  it  is  there- 
fore not  applicable  to  the 
combined  counting  of  red  and 
white  cells. 


Hayem's  Solution  consists  of: 

Bichloride  of  mercury.     0.5 

Sodium  sulphate 5.0 

Sodium    chloride! 1.0 

Distilled  water 200.0 


Toisson's   Fluid   consists  of: 


Sodium  chloride.  . 
Sodium  sulphate . , 
Neutral  glycerine, 
Distilled  water. .  , 
Methyl  violet  5  B, 


1.0    G. 

8.0    G. 
30.0    c.c. 
160.00  c.c. 
.025  G. 


This  colors  the  white  cells 
and  with  it  both  red  and 
white  cells  can  be  counted. 
Objections  to  this  fluid  are 
(1)  it  may  cause  hemolysis  at 
times;  hence  the  red  count  is 
worthless;  (2)  spores  develop 
readily  in  it  and  in  order  to 
use  it  must  flrst  be  filtered. 
Each  filtration  further  weak- 
ens the  solution. 

COLOR  INDEX.     (Value  of  corpuscles.) 

Represents  the  relative  amount  of  hemoglobin  con- 
tained in  each  red  cell  as  compared  when  a  normal  num- 
ber of  erythrocytes  obtains.  In  other  words,  it  is  the 
quotient  of  the  percentage  of  Hb.  divided  by  the  per- 
centage red  cells.  The  latter  factor  is  obtained  by  divid- 
ing the  number  of  red  cells  counted  by  5  million. 

Examples: 

What  is  the  color  index  when  one  counts  2,500,000 
red  cells  and  the  Hb.  is  50%? 


2,500,000 


^  14  =  50%;  and 


50 


1  =  Color  Index. 


5,000,000       '"  '  50 

What  is   the   color  index  when  one   counts   3,000,000 
red  cells  and  the  Hb.  is  40%  ? 


3,000,000 
5,000,000 


—  3/. 


2.L 


60%;  and 


38 


40 
60 


%  =  Color  Index. 


What  is  the  color  index  when  one  counts  1,500,000 
red  cells  and  the  Hb.  is  45%? 

1,500,000     ,,  _^.  ,45       _.        ^  ,       ^    . 

-^^^^^^=.Vio  =  30%  ;   and  -  =  IV.  =  Color  Index. 

A  very  simple  method  of  obtaining  the  percentage  of 
red  cells  of  the  normal  5,000,000  is  to  multiply  the  num- 
ber of  hundreds  of  thousands  of  the  red  cells  counted  by 
two.  Thus  if  2,650,000  cells  were  counted,  we  multiply 
265  by  2.     This  equals  53%. 


WHITE  BLOOD  CORPUSCLES. 
(LEUCOCYTES.) 

MORPHOLOGY.  In  the  fresh  specimen,  they  appear  as 
highly  refractive,  nucleated  cells,  having  a  variable 
amount  of  clear  or  granular  cytoplasm,  possessed  of 
ameboid  movement  with  a  phagocytic  property.  They 
are  larger  than  the  R.  B.  C. 

CLASSIFICATIONS. 

1.  Mixed  or  present  classification  of  today: 

(a)  Polymorphonuclear  neutrophile. 

(b)  Lymphocytes:    large  and  small. 

(c)  Mononuclear. 

(d)  Transitional. 

(e)  Polynuclear  eosinophile. 

(f)  Polynuclear  basophile    (mast  cell). 

2.  According  to   granules: 

f  Polymorphonuclear  neutrophile. 

(a)  Granular  }  Eosinophile. 
(a j     trranuiar <;^  Basophile. 

1^  Myelocyte. 

r  Lymphocytes. 

(b)  Non-granular  ..<  Mononuclear. 

i  Transitional. 

3.  According  to   nuclei: 

{Neutrophile. 
Eosinophile. 
Basophile. 

(b)     Mononuclear.  .  .  .AH  the  rest. 

4.  According    to    staining    of    protoplasm: 

(a)  Neutrophile. 

(b)  Eosinophile. 

(c)  Basophile. 

39 


LEUCOCYTES    DESCRIBED. 

(a)  POLYMORPHONUCLEAR  NEUTROPHILE.    (Finely 
granular  cells  of  Scliultze.) 

Constitute   65   to   75%    of  the  total  white   cells. 

Twice  as  large  as  a  red  cell. 

Nucleus  or  rather  nuclei  vary  greatly  in  shape 
and  are  stained  blue   (basophilic). 

Protoplasm  contains  numerous  irregularly  placed 
and  irregular  sized  granules  stained  pink  (acido- 
philic). 

When  outside  the  blood  vessels  they  form  pus. 

(b)  LYMPHOCYTES. 

Constitute  20  to  30%   of  the  total  W.  B.  C. 
Large    lymphocyte. 

One  and  one-half  times  the  size  of  R.  B.  C. 

Nucleus  deeply  stained. 

Has  more  cytoplasm  than  a  small  lymphocyte. 
Small    lymphocyte. 

Is  about  the  size  of  a  red  cell. 

Its  nucleus  also  deeply  stained. 

Has  a  small  rim  of  cytoplasm. 

(c)  LARGE   MONONUCLEAR. 

About  3  times  as  large  as  a  red  cell. 

Has  a  round  or  oval  faintly  stained  nucleus, 
which  is  basophilic. 

Considerable  reticulated  cytoplasm,  few  meta- 
chromatic granules. 

(d)  TRANSITIONAL. 

(c)    plus    (d)    equal    6%    of   the   total   W.    B.    C. 
These  cells  resemble  the  former  excepting  that 
the  nuclei  are  kidney  shaped   (notched)   and  pale. 

(e)  POLYMORPHONUCLEAR  EOSINOPHILE.    (Coarse- 
ly granular  cells  of  Schultze.) 

Constitute  about  one-half  to  3%  of  total  W.  B.  C. 

Is  as  large  as  a  polymorphonuclear  cell. 

Has  large,  coarse,  red  granules  arranged  in 
mosaic  form  in  its  protoplasm.  It  stains  with  acid 
dyes.  The  nuclei  are  coarsely  reticulated,  usually 
bilobed,  and  rather  indistinct, 

40 


{For  Drawings) 


41 


(f)  POLYMORPHONUCLEAR  BASOPHILE  OR  MAST 
CELL. 

Constitutes  one-half  per  cent,  of  total  W.  B.  C. 
Is  as  large  as  a  polymorphonuclear  cell. 

Nucleus  is  indistinct. 

Cell  appears  as  if  it  were  bespattered  with  ink. 
It  also  has  metachromatic  granules. 
The   mast   cells    are   best   stained   by   Ehrlich's 
dahlia  stain  or  by  Turk's  iodine  method. 

NUMBER   OF   LEUCOCYTES. 

Normally:    5,000  to  10,000  per  c.mm.     Average  7,500. 
Leucopenia:    Reduction  in  total  white  count. 
Leucocytosis:    Increase  in  total  white  count.     May  be 

(a)  Absolute:    Increase  in  total  number  of  W.  B.   C. 

(b)  Relative:  A  proportionate  increase  of  any  given 
variety  of  colorless  corpuscles,  the  total  white  count 
remaining  unaltered. 

CLASSIFICATION  OF  LEUCOCYTOSES  (Modified  after  Lim- 
beck) . 

1.  PHYSIOLOGICAL  LEUCOCYTOSIS. 

(a)  Digestive.  Unless  cancer  of  the  stomach  exists 
a  leucocytosis  of  the  polynuclear  type  averaging 
10,000  occurs  after  eating. 

(b)  Pregnancy.     Average  count  is  15,000. 

Occurs  in  more  than  50  9o  of  the  cases. 
Especially  marked  in  primiparse. 

All  the  white  cells  excepting  eosinophiles 
are  increased.      (Mixed  leucocytosis.) 

Count  returns  to  normal  within  10  to  14 
days  after  delivery  providing  no  such  complica- 
tions like  fever,  hemorrhage,  etc.,  arise. 

(c)  New-born.    Average  15  to  20  thousand. 

Disappears  as  child  begins  to  gain  in  weight. 

The  small  mononuclears  constitute  40  to 
60%  of  total  W.  B.  C. 

2.  PATHOLOGICAL  LEUCOCYTOSIS. 

(a)  Inflammatory.  All  forms  of  suppurative  inflam- 
mation except  when  an  abscess  is  well  walled 
off.  In  septic  conditions  the  polymorphonuclear 
cells  predominate. 

42 


The  common  diseases  associated  with  leuco- 
cytosis  are:  acute  lobar  pneumonia,  acute  articu- 
lar rheumatism,  scarlet  fever,  whooping  cough, 
erysipelas,  cerebro-spinal  meningitis,  pus  infec- 
tions,  etc. 

(b)  Cachectic   (due  to  malignant  tumors). 

More  often  after  cancer  than  sarcoma. 

(c)  Posthemorrhagic.  Polymorphonuclear  cells  pre- 
dominate. White  count  may  reach  20,000  w^ithin 
one  hour  after  a  severe  hemorrhage.  It  is,  how- 
ever, transient,  disappearing  long  before  regen- 
eration of  the  blood  has  occurred. 

3.  Leucocytosis    from    medicinal   and   therapeutic   meas- 
ures:   baths,  drugs,  exercise. 

4.  Leucocytosis  from  other  causes:    cyanosis,  shock,  vac- 
cine injections,  etc. 

IVIIXED    LEUCOCYTOSIS. 

An  increase  in  both  granular  and  non-granular  cells 
but  its  more  common  interpretation  is  an  increase  in 
the  number  of  neutrophile  myelocytes.  Best  seen  in 
spleno-myelogenous  leukemia.  In  no  other  conditions 
excepting  leukemia  do  we  ever  find  more  than  1,000  mye- 
locytes.    In  leukemia  it  may  reach  150,000. 

SIGNIFICANCE  OF  RELATIVE  LEUCOCYTOSES. 

EOSINOPHILIA.     To  be  called  a  true  eosinophilia  there 
must  be  over  250  such  cells  per  c.mm. 

(a)  Parasitic  infections:  as  trichinosis,  intestinal  worms, 
hydatids,  chronic  malaria. 

(b)  Bronchial  asthma  at  time  of  paroxysm. 

(c)  Spleno-myelogenous  leukemia. 

(d)  Many  skin  diseases.  Seems  to  depend  more  upon 
extent  of  lesions  than  upon  nature.  Common  dis- 
eases are:  pemphigus,  urticaria,  purpura,  eczema, 
psoriasis. 

(e)  Bone  diseases:  osteomyelitis,  osteomyalacia,  sar- 
coma. 

(f)  Malignant  disease. 

(g)  Gonorrhea:  both  in  blood  and  discharge. 

LYMPHOCYTOSIS. 

(a)  Children.  From  birth  up  to  puberty  the  lymphocytes 
constitute  50  to  65 9^  of  W.  B.  C.  Gradual  reduction 
to  the  normal  20  to  30 7o  by  the  time  puberty  is 
reached. 

43 


(b)  Lymphatic  leukemia. 

Acute   forms:     large   lymphocytes   predominate. 
Chronic  forms:   small  lymphocytes  predominate. 

(c)  Typhoid.    Uncomplicated  cases  show  leucopenia  with 
lymphocytosis. 

(d)  Syphilis.    Also  found  in  the  spinal  fluid  in  syphilitics. 

MYELOCYTOSIS.  A  myelocyte  is  a  mononuclear  cell  which 
is  distinctly  granular.  These  granules  are  usually  neu- 
trophilic or  eosinophilic.  But  in  myelogenous  leukemia 
they  may  be  basophilic.  The  size  of  myelocytes  varies 
from  that  of  a  R.  B.  C.  to  a  large  mononuclear.  The 
myelocytes  are  not  normally  found  in  the  circulation 
but  they  are  found  in  the  bone-marrow. 

(a)  Spleno-myelogenous  leukemia. 

(b)  Pernicous  anema. 

(c)  Bone   disease:     syphilis,  tuberculosis,  tumors. 

(d)  Malignant  tumors  of  gastro-intestinal  tract. 

(e)  Empyema  in  children. 

(f)  Some  acute  infectious  diseases: 

Lobar  pneumonia   (8  to  12 7o). 
Diphtheria:       (bad  prognosis). 

LEUCOPENIA.     White  count  reduced  below  5,000. 

(a)  Typhoid:    uncomplicated  cases  only. 

(b)  Measles:    after  the  rash. 

(c)  Malaria:    but  lymphocytes  may  be  slightly  increased. 

(d)  Tuberculosis. 

(e)  Mumps  unless  suppuration  of  the  gland  occurs. 

(f)  Starvation  and  malnutrition. 

(g)  Chronic  poisoning  with  heavy  metals,  morphine,  al- 
cohol, cocaine. 

(h)     Grippe   if  uncomplicated.     Thus,   can   be   diagnosed 

from  pneumonia  in  which  leucocytosis  occurs. 
(i)      Pernicious  anemia  and  splenic  anemia. 

COUNTING  THE  WHITE   CELLS. 

Draw    blood   up   to    0.5    mark   in    pipette    No.    11. 

Draw  up  sufficient  amount  of  0.5%  acetic  acid  solu- 
tion up  to  the  11  mark.     (Acetic  acid  destroys  R.  B,  C.) 

Examine  as  described  under  red  cells  (page  37),  but 
count  the  entire  400  squares  and  use  low  power  lens. 

The  dilution  as  given  above  is  20. 

44 


To  find  the  number  of  W.  B.  C.  multiply  the  number 
of  cells  counted  in  all  the  squares  by  20  and  then  by  10 
(the  depth  of  the  examining  chamber).  In  other  words, 
multiply  the  number  of  cells  counted  by  200. 

If  blood  be  drawn  past  the  0.5  mark,  divide  the  num- 
ber of  cells  counted  by  the  division  at  which  we  stopped 
and  multiply  by  100. 

Suppose  we  counted  42  cells  in  0.6  c.c.  blood.     There- 
fore ^  X  100  =  7,000   W.   B.   C. 
O.b 

DIFFERENTIAL  WHITE  COUNT. 

First   ascertain   the  total   white   count   as   above. 

Make  a  thin  blood  smear,  fix,  stain  and  examine  with 
a  microscope.  (Wright's  stain  is  best  for  differential 
count). 

Count  200  leucocytes  and  as  each  one  is  seen  place 
a  mark  along  the  side  of  the  name  of  the  cell  in  the  list 
as  arranged  below: 

Polymorphonuclear  neutrophile. 
Large  lymphocyte. 
Small  lymphocyte. 
Mononuclear. 
^   Transitional. 

Polymorphonuclear  eosinophile. 
Polymorphonuclear  basophile. 
Unclassified  cells. 
Pathological  cells. 

Now  then,  assuming  that  150  polymorphonuclear  neu- 
trophiles  were  counted  in  the  200  squares  the  percentage 
therefore  is  75.  The  percentages  for  the  other  cells  are 
determined   in  a   similar  manner. 

BLOOD  SMEARS:    Preparation  and  staining. 

Cleanse  part  from  which  blood  is  to  be  drawn. 

Puncture  skin  with  a  Hagerdorn  needle  and  wipe  off 
the   first   drop   of   blood   which  appears. 

Apply  a  clean  slide  to  the  bleeding  point  and  permit 
one  drop  to  adhere  to  the  slide  at  a  point  about  %-inch 
from  the  smaller  edge  of  the  oblong  slide. 

With  another  clean  slide,  held  at  an  angle  of  45% 
bisect  this  drop  and  wait  until  the  blood  has  spread  along 
this  angle  by  capillarity. 

45 


When  the  angle  has  almost  completely  been  covered 
draw  the  second  slide  across  the  first  using  firm  and 
steady  pressure.     The  object  is  to  get  a  thin  smear. 

Before  any  of  the  morphological  elements  of  the 
blood  can  take  up  any  stain  the  smear  must  first  be 
FIXED  by  any  process  which  will  coagulate  the  proteid 
constituent  of  the  blood. 

The  air  dried  film  is  exposed  to  heat  or  to  chemicals. 
Fixation  by  methyl  alcohol  (C.  P.)  for  3  to  5  minutes  is 
one  of  the  best  methods. 

STAINS   FOR   ROUTINE   PURPOSES. 

f      These    stains   are   the   best 

1.  Eosin-methylene  blue.    |  because    they    are    simple    in 

2.  Eosin-hematoxylin.         ■{  technic    and    show    clear-cut 

3.  Wright's  stain.  |  pictures  of  all  the  important 

[  blood  elements. 

1.      EOSIN-METHYLENE  BLUE  STAIN. 

1.  Fix  smear  in  pure  methyl  alcohol  for  3  minutes 
(If  we  find  later  that  the  nuclei  are  indistinct  fix 
for  a  longer  period.) 

2.  Stain  in  i^'/o  alcoholic  (709o)  solution  of  Grubler's 
"French  pure"  eosin  for  3  to  5  minutes.  (This 
brings  out  the  neutrophilic  granules  distinctly). 

3.  Wash  in  distilled  water  and  dry  between  filter 
paper. 

4.  Deposit  slide  for  %  to  1  minute  in  a  small  bath 
containing: 

20  drops  of  a  %9o  aqueous  solution  of  methy- 
lene blue  (B.  pat),  and 
10  drops  of  the  above  eosin  solution. 

5.  Quickly  w^ash   (briefly)  w4th  distilled  water. 

6.  Dry  at  once  between  filter  paper  or  over  flame. 

7.  Mount  if  desired  in  Canada  Balsam  or  examine  di- 
rectly with  high  power  lens. 

With  this  stain  the  morphological  elements  are 
thusly  recognized: 

R.  B,  C.  and  eosinophilic  granules  of  W.  B.  C: 
bright  red. 

Neutrophilic  granules:     pink  to  bright  red. 

(The  granules  being  smaller  than  that  of  the 
eosinophiles.) 

46 


Nuclei,  mast-cell  granules,  bodies  of  lym- 
phocytes, platelets,  malarial  organisms,  trypano- 
somes  and  filaria:    varying  shades  of  blue. 

Note. — For  malaria  it  is  not  a  very  good 
stain  because  it  does  not  stain  the  chromatin  very 
good.  It  is  better  than  any  of  the  Romanowsky's 
stains  or  its  modifications. 

2.      EOSIN    HEMATOXYLIN  STAIN. 

Best  adapted  for  examination  of  nuclear  structures. 
Two  solutions  are  required. 

Stain  with  solution  No.  1  for  i^  minute. 

Wash  in  water  but  do  not  dry. 

Deposit  slide  in  solution  No.  2  for  1  to  3  minutes. 

Wash  in  water,  dry  and  mount. 

Solution  No.  1.     ^%  Griibler's  blood  eosin  in  70% 
alcohol. 

Solution    No.   2.     Delafield's  hematoxylin  solution 

which  consists  of: 

Hematoxylin  crystals 4  G. 

Absolute   alcohol 25  c.'c. 

Ammonium-alum  crystals  C.  P...'.".'.'.*  52  G. 

Distilled  water 400  c.c 

Glycerine,  C.  P .' '  * ,'  ,'ioo  c  c 

Methyl  alcohol,  C.  P *...*.'.'.  100  c.c! 

HOW  TO   PREPARE   DELAFIELD'S   HEMATOXYLIN   SOLU- 
TION : 

1.  Rub    up    hemotoxylin    crystals    with    alcohol    until    dis- 

o Ol  V  GO. , 

2.  Place  this  solution  in  a  loosely  corked  bottle  and  ner- 
mit   to   stand   4   days   exposed   to   the   lig-ht. 

3.  Dissolve  the  ammonium-alum  crystals  in  400  c  c  water 
and  allow  to  stand  as  the  above.  "  ' 

4.  After  4  days  mix  both  bottles  and   shake  vigorously 

5.  After  3   hours,   filter. 

6.  Now  add  the  glycerine  and  methyl  alcohol  to  the  filtrale 
and  allow  this  to  stand  over  night.  mxraice 

7.  Filter  this  mixture  again,  catching  the  filtrate  in  a 
clear  bottle.  After  standing  in  the  light  for  six  weeks 
It   ripens   and   is   ready   for   use. 

3.     WRIGHT'S  STAIN. 

1.  Flood  the  smear  with  the  stain  for  one  minute  A 
definite  number  of  drops  should  be  dropped  on  the 
slide    by  means  of  a  medicine  dropper. 

47 


2.  Add  the  same  number  of  drops  of  distilled  water. 
(See  that  no  fluid  runs  off  by  using  proper 
amounts.)  (It  stains  the  eosinophilic  granules 
beautifully.) 

3.  Wash  in  water  for  30  seconds,  or  until  the  thinner 
portion  of  the  film  becomes  yellow  or  pink. 

4.  Dry  between  filter  paper;  mount  if  desired  and 
examine. 

Note. — for  malarial  parasites  the  decoloriza- 
tion  should  not  be  so  long  because  it  affects  the 
chromatin. 

The  formed  elements  are  thusly  colored: 

R.  B.  C orange  or  pink. 

Nuclei  of  W.  B.  C blue  or  dark  lilac. 

Neutrophilic  granules lilac. 

Eosinophilic  granules red  or  pink. 

Fine  basophilic  granules deep  blue. 

Large  mast-cell  granules. purple 

Protoplasm  of  lymphocytes robin's-egg  blue. 

Bacteria blue. 

Malarial  and  other  parasites blue. 

(The   chromatin   elements   varying   from   lilac 
to  ruby-red  to  black.) 

Polychromatophilia  and   granular   degenera- 
tions. .  .  .: blue. 

PREPARATION   OF  WRIGHT'S  STAIN. 

Place  into  a  suitable  flask  1  G.  methylene  blue  (B.  X. 
or  "medicinally  pure")  for  every  100  c.c.  of  0.5%  solution 
of   sodium    bicarbonate. 

Heat  this  mixture  for  60  minutes  in  a  steam  sterilizer 
at   100°    C.      After   heating,   permit   to   cool. 

Filter    a.nd    remove    tlie    precipitate. 

To  each  100  c.c.  of  the  filtered  mixture  add  500  c.c.  of 
a  0.1 '/o  aqueous  soltition  of  "yellowish,  water-soluble" 
eosin    and    mix    thoroughly. 

Collect  the  abundant  precipitate  (which  appears  im- 
mediately)   on  a   filter. 

When  this  precipitate  is  dry  dissolve  in  methyl  alcohol 
(Merck's  reagent)  in  the  proportion  of  0.1  G.  to  60  c.c.  of 
alcohol. 

This  is  the  stain  and  should  be  kept  well  stoppered  to 
prevent  evaporation  of  the  alcohol. 


HEMOGLOBIN.     (Hb.) 

A  complex  proteid  containing  iron.  It  is  the  pigment 
which  gives  color  to  the  blood.  It  forms  loose  combina- 
tions with  oxygen  and  plays  an  important  part  in  res- 
piration. 

AMOUNT.  For  every  100  c.c.  blood  we  find  on  an  average  of 
13.77  G.  Hemoglobin  (symbol  Hb.).  In  man  it  is  nearer 
to  14  G.     In  women  it  is  nearer  13  G. 

Clinically  14  G.   is  regarded  as  lOC/V. 

The  estimation  of  the  percentage  hemoglobin  is  ar- 
rived at  by  comparing  the  color  of  that  patienfs  blood 
to  certain  standard  solutions  of  blood  or  standardized 
color  charts  or  scales.  The  hemoglobinometers  recom- 
mended are  Pleischl-Miescher's,  Sahli's,  Gower's,  Dare's, 
Oliver,  Tallqvist's,  etc. 

(The  reader  is  now  referred  to  page  38  for  the  dis- 
cussion of  "color-index,"  and  to  Schmaltz's  figures  for 
percentage   Hb.   based   upon   specific   gravity.     P.   33.) 

HEMOGLOBINEMIA  AND   HEMOGLOBINURIA. 

Normally  red  cells  are  being  constantly  disintegrated 
but  is  very  insignificant. 

Under  certain  conditions  the  destruction  is  so  rapid 
and  the  blood  pigment  accumulates  so  rapidly  in  the  blood 
(hemoglobinemia)  that  the  liver  is  unable  to  convert  it 
into  bilirubin.  With  hemoglobinemia  there  must  be 
hemoglobinuria  (the  pigment  passes  out  through  the 
urine). 

It  may  occur  In  the  following  conditions: 

1.  Poisoning.  Phenol,  chlorate  of  potash,  pyrogallic  acid, 
antimony,  hydrochloric  ,and  sulphuric  acids,  coal-tar 
products,  sulphonal,  etc.,  either  by  hypodermic  injec- 
tions or  large  doses  internally. 

2.  Certain  diseases.  Scarlatina,  typhoid,  intermittent 
fever,  icterus  gravis,  syphilis. 

3.  After  transfusions  of  the  blood  of  animals  into  man, 
and  after  severe  burns  and  exposure  to  cold. 

4.  Anesthetics  are  also  hemolytic  poisons. 

Urine.  The  urine  in  hemoglobinuria  is  usually 
turbid.  Varies  in  color  from  bright  red  to  almost 
black.  It  must  not  be  confounded  with  hematuria. 
Chemical    tests    cannot    differentiate     them.       Micro- 

49 


/     J 


scopically  in  hematuria  we  find  the  red  blood  cells. 
In  hemoglobinuria  the  urine  should  be  immediately 
centrifuged.  Few  or  no  red  cells  should  be  in  the 
sediment, 

TESTS  FOR   HEMOGLOBIN  AND  DERIVATIVES. 

(A)  HELLER'S  TEST. 

1.  Add  NaOH  to  a  few  c.c.  of  urine  so  as  to  make 
it  strongly  alkaline. 

2.  Heat.  A  brownish-red  precipitate  is  thrown 
down.  Color  due  to  the  presence  of  hematin. 
Precipitate  consists  of  the  phosphates  and  car- 
bonates of  the  alkaline  earths. 

3.  In  case  the  urine  contains  a  large  amount  of 
foreign  pigment,  the  red  cells  may  not  be 
easily  noted. 

In  that  case,  filter  off  the  precipitate  and 
redissolve  it  in  acetic  acid.  In  the  presence  of 
blood  it  becomes  red  but  fades  on  standing  in 
the  air. 

Note. — This  test  will  indicate  one  part  oxy- 
hemoglobin in  4,000  urine. 

(B)  DONOGANY'S    TEST. 

1.  To  10  c.c.  urine  add  1  c.c.  ammonium  sulphide 
and  1  c.c,  pyridin.  In  the  presence  of  blood 
the  urine  becomes  orange-colored, 

2.  Hemoglobin  having  thus  been  converted  into 
hemochromogen  we  can  recognize  same  by  its 
characteristic  absorption  bands.     (See  page  94.) 

3.  This  test  shows  one  part  blood  to  8,000  of  urine. 

4.  If  the  urine  contains  fresh  blood,  the  spectrum 
will  be  that  of  oxyhemoglobin  while  in  case  of 
hemoglobinuria  or  of  hematuria  of  renal  origin, 
the  spectrum  is  that  of  methemoglobin.  (Web- 
ster,) 

5.  For  the  spectroscopic  examination  of  urine  it  is 
necessary  that  the  urine  be  acid, 

PAROXYSMAL  HEMOGLOBI  NEMIA. 

1.  Cause  is  unknown  but  usually  follows  catching  cold. 

2,  Attack  is  paroxysmal  and  ushered  in  by  persistent 
yawning,  pain  in  limbs,  headache,  nausea  and  vomit 
and  coolness  of  the  periphery, 

50 


3.  Temperature  quickly  rises   to   102"   and   is   associated 
with  a  severe  chill. 

4.  Severe  hepatic  pains  at  times. 

5.  Splenomegaly  very  characteristic. 

6.  Slight  jaundice  towards  end  of  the  attack. 

7.  After  10  to  12  hours,  the  fever  falls  and  is  followed 
by  sweating. 

8.  Urticarial    eruptions    frequently    seen    during    attack. 

9.  Urine  very  characteristic.     (During  and  directly  after 
the  paroxysms.) 

Color:    varies   from   brownish-red   color   to   black. 
Reaction:    invariably  acid. 

Specific  gravity:    usually  low:    1008-1012. 

Boiling:  will  decompose  the  Hb.  and  a  brown 
coagulum  of  albumen  is  formed. 

Spectroscopy:  fresh  urine  shows  Hb.  spectrum 
and  sometimes  that  of  methemoglobin. 

Casts:  usually  present.  (Hyaline  and  some  con- 
taining hemoglobin  granules.) 

NO  RED  BLOOD  CELLS  ARE  FOUND  IN  THE 
URINE. 

10.     Blood  during  the  paroxysm. 

Tendency  to  "coin-roil '  formation  less  marked. 

R.  B.  C.  pale  and  often  devoid  of  color. 

Poikilocytosis. 

If  blood  be  withdrawn  and  allowed  to  clot,  the 
serum  which  exudes  will  be  red-tinted  instead  of 
straw  colored  as  normally. 


HEMOLYSIS. 

DEFINITION. 

The  dissolution  of  the  red  cells  with  the  passing  out 
of  its  hemoglobin  into  the  plasma  or  other  medium  in 
which  the  R.  B.  C.  are  suspended. 

Hemolysis  may  be  produced  by  certain  physical 
agents:  distilled  water,  freezing  and  thawing,  tempera- 
ture of  55°   C.  for  30  minutes. 

It  may  also  be  brought  about  by  certain  chemical 
agents:  most  organic  acids,  mineral  acids,  all  alkalies, 
bile  salts,  bichloride  of  mercury,  etc. 

51 


Also  by  animal  venoms:    snakes,  bees,  spiders,  etc. 

Hemolysis  by  serum.     This  is  quite  different  from  hemoly- 
sis caused  by  the  above  forces. 

The  serum  of  one  animal  may  be  hemolytic  to  the  red 
cells  of  another  or  several  animals.  Its  action  depends 
upon  the  presence  of  two  substances  in  the  serum:  am- 
boceptor and  complement,  both  being  mutually  dependent 
upon  each  other  in  the  process  by  which  the  red  cells  are 
destroyed.  IT  FORMS  THE  BASIS  OF  THE  SERUM 
DIAGNOSIS  OF  SYPHILIS.      (See  p.  71.) 

The  red  cells  float  in  the  plasma  which  has  an  os- 
motic pressure  the  same  as  that  which  exists  within  the 
red  corpuscles.  It  is  only  when  the  osmotic  pressure  be- 
tween plasma  and  corpuscles  are  disturbed. that  hemolysis 
can  occur. 

If  red  cells  are  suspended  in  a  normal  physiological 
salt  solution  (0.9 7f  NaCl)  which  is  isotonic  with  that  of 
the  blood,  hemolysis  will  not  occur. 


COAGULATION  OF  THE  BLOOD. 

NORMAL  COAGULATION  TIME.      (HEMATOPEXIS.) 

Within  2  to  8  minutes  after  the  blood  leaves  the  blood 
vessel  it  clots  or  coagulates. 

After  9  minutes,  it  is  called  delayed  coagulation. 

COAGULATION  TIME  IS  DELAYED  IN: 

Anemia.  Scurvy,  Hemoglobinemia, 

Jaundice,  Hemophilia,  Cobra  bite. 

Anasarca,  Asphyxia, 

Purpura,  Toxemias, 

COAGULATION   OCCURS  QUICKER   IN: 

Conditions  associated  with  stasis. 

Repeated  hemorrhages. 

Transfusions. 

Hunger. 

After  using  calcium  chloride,  coagulose.  horse-serum, 
gelatin. 

TESTS  FOR  COAGULATION  TIME: 

1.     Several  drops  of  blood  are  allowed  to  fall  on  a  clean 
slide. 

52 


At  intervals  of  one  minute  a  broom  straw  or 
white  horse  hair  (which  has  previously  been  boiled  in 
alcohol  and  ether)  is  drawn  lightly  through  each  drop 
until  a  thread  of  fibrin  is  seen  clinging  to  the  straw  or 
hair.     This  is  a  rough  method. 

2.  Rudolph's  Method.  (Reader  referred  elsewhere).  This 
is  more  accurate.  The  normal  coagulation  time  with 
this  method  is  8^/^  minutes. 

Intravascular  clotting. 

Blood  never  clots  within  a  normal  blood  vessel 
under  normal  circumstances. 

Intravascular  clotting  may  be  hastened  by  the  in- 
troduction into  the  blood  stream  of  foreign  bodies  or 
air  which  cause  thrombi;  or  by  injuring  the  endo- 
thelium of  the  arterial  wall;  by  the  injection  of 
macerated  lymph  gland  or  horse  serum,  etc. 

Methods  of  preventing  extravascular  clotting: 

1.  Freezing,  which  destroys  the  enzymes. 

2.  Drawing  blood  into  concentrated  magnesium  sulphate 
solution.     It  combines  with  calcium. 

3.  Sodium  oxalate   (0.1%   sol.).     Combines  with  calcium. 

4.  Sodium  fluoride. 

5.  Drawing  blood  into  an  oiled  vessel  and  stirring  with 
an  oiled  rod. 


i 


PHYSIOLOGY   AND   CHEMISTRY   OF 
CLOTTING. 


-r,     ,,          v.-     ,    r          thrombokinase  Thrombin 

Prothrombin -|-  J  

zymoplastic  substances     fibrin  ferment 


Calcium  salt-j-  1 


(^  Thrombin -|-fibrinogen=fibrin  (the  clot). 
Explanation  of  these  equations: 

Prothrombin.  Is  inactive.  Exists  in  the  blood  as  a  pre- 
cursor of  thrombin,  just  as  inactive  trypsinogen  is  a 
precursor  of  trypsin. 

Calcium  salts.  When  absent  clotting  will  not  occur.  It 
can  readily  be  proven  by  adding  ammonium  oxalate 
to  precipitate  the  calcium. 


/^' 


Thrombokinase.  Derived  from  the  tissues,  the  blood 
plates  or  the  corpuscles  and  are  the  agency  by  which 
inactive  prothromhir  is  converted  into  active  throm- 
bin in  the  presence  of  calcium  salts. 

Fibrinogen.  A  normal  constituent  of  all  blood  plasma. 
This  reacts  with  the  newly  formed  thrombin  and 
forms  the  clot  which  is  called  fibrin. 

Fibrin  (Clot).  The  clot  is  a  network  of  fibrin  in  the 
plasma.  In  the  meshes  of  the  clot  many  red  cells 
are  entangled.  The  network  is  oftentimes  seen  to 
radiate  from  the  blood  plates. 

When  blood  is  first  drawn  into  a  vessel  it  be- 
comes transformed  into  a  semi-solid  gelatinous  mass. 
Later,  the  clot  shrinks  and  a  straw-colored  liquid 
(plasma)  collects  at  the  top. 

Plasma  differs  from  serum  in  that  it  does  not 
contain  fibrinogen  which  was  consumed  during  coagu- 
lation. 


54 


CHAPTER  III. 

EXAMINATION  OF  THE  BLOOD  FOR  BAC- 
TERIA AND  PARASITES. 

TAKING  BLOOD  FROM  A  VEIN  FOR  CULTURE  PURPOSES. 

1.  Ten  c.c.  of  blood  is  withdrawn  from  the  median  basilic 
vein  by  means  of  a  sterile  Liier  syringe. 

2.  Transfer  this  blood  immediately  to  an  Erlenmeyer 
flask  containing  1.50  c.c.  broth  (either  plain  or  1% 
glucose)  and  shake. 

3.  Incubate  for  36  hours  at  a  temperature  of  37'   C. 

4.  Shake,  remove  1.5  c.c.  and  place  into  a  centrifuge. 

5.  After  20  minutes  centrifuging,  decant  the  supernatent 
liquid   and   with   the   sediment  inoculate   agar   slants. 

TYPHOID    FEVER. 

1.  The  bacilli  may  be  isolated  from  the  blood  even  when 
a  Widal  reaction  may  not  be  positive. 

2.  Of  the  10  c.c.  blood  taken  for  culture  purposes,  place 
1  c.c.  into  each  of  2  Erlenmeyer  flasks  containing 
150  c.c.  broth  and  into  2  more  such  flasks  place  2  c.c. 
blood.  We  thus  have  2  flasks  with  a  dilution  of  1:150 
and  2  more  with  a  dilution  of  1:75. 

3.  Incubate  for  24  to  36  hours. 

4.  Make  a  hanging  drop  examination  for  motile  bacilli. 
If  negative  incubate  for  another  24  hours. 

5.  When  the  bouillon  has  become  cloudy,  make  sub- 
cultures in  milk  and  glucose  bouillon  and  test  again 
with  an  actively  agglutinating  serum. 

Another  method. 

1.  Add  blood  to  sterilized  ox  bile  in  proportion  of  1  c.c. 
blood  to  5  c.c.  ox  bile, 

2.  Incubate  12  to  15  hours  at  37°  C. 

3.  Transfer  a  few  loop  fulls  to  either  the  Drigalski-Con- 
radi  or  the  Modified  Endo  Media. 

4.  The  colonies  which  then  develop  are  then  subcultured 
and  agglutination  tests  made. 


55 


With  these  media,  positive  agglutination  tests 
are  absolutely  diagnostic  of  typhoid.  No  germs  are 
found  in  the  blood  after  the  third  week. 

Widal    Reaction.      (See  p.   69.) 

PNEUMONIA. 

1.  The  finding  of  the  diplococcus  of  Fraenkel  in  the  blood 
has  more  of  a  prognostic  than  diagnostic  value. 

2.  Fraenkel  claims  that  if  1  c.c.  of  the  patient's  blood 
be  spread  on  agar  plates  and  a  luxuriant  growth  of 
colonies  develop,  we  may  infer  that  death  from  sepsis 
may  occur  or  else  metastasis  to  other  organs  may  take 
place. 

3.  On  the  other  hand,  if  the  growth  be  small,  and  it  be- 
comes necessary  to  take  larger  volumes  of  blood  to 
demonstrate  the  presence  of  diplococci  and  to  grow 
them  in  bouillon  instead  of  agar,  the  prognosis  is  much 
better. 

4.  The  organisms  can  be  demonstrated  as  early  as  12 
hours  after  the   initial   congestive   chill. 

5.  The  rule  is  that  the  diplococci  disappear  after  the 
crisis. 

6.  Instead  of  using  agar,  Rosenow  uses  blood  agar.  The 
diplococci,  when  grown  on  blood  agar  plates  produce 
greenish  hemolytic  zones.  This  distinguishes  the 
pneumococcus  from  the  streptococcus  pyogenes  which 
causes  hemolysis  without  pigment  production. 

7.  Rosenow  also  has  a  special  stain  to  bring  out  the  cap- 
sule of  the  pneumococcus. 

ANTHRAX. 

1.  The  bacilli  are  usually  present  in  such  large  numbers 
that  they  may  be  found  by  simply  making  and  stain- 
ing a  blood  smear. 

2.  The  stain  consists  of: 

Concentrated  sol.  methylene  blue 30  c.c. 

Potassium  hydrate  sol.  (1:10,000) 100  c.c. 

3.  Stain  with  this  for  5  or  10  minutes. 

4.  Wash  in  0.5 9'c  acetic  acid  sol.  for  10  seconds. 

5.  Wash  in  alcohol  and  dry. 

In  doubtful  cases,  a  guinea-pig  should  be  injected 
with  some  of  the  patient's  blood,  and  if  anthrax  be 
present  a  luxuriant  growth  takes  place  in  this  animal. 

56 


GONORRHEAL    INFECTIONS. 

1.  Neisser's  organisms  may  be  found  in  the  blood  in  cases 
associated  with  gonorrheal  involvement  of  the  endo- 
cardium, joints,  etc. 

SEPTICEMIA   AND   PYEMIA. 

1.  Streptococci  may  be  found  in  the  blood  especially 
when  the  endocardium  is  involved. 

2.  These  germs  form  typical  chain-like  growths. 

3.  In  doubtful  cases,  one  c.c.  of  venous  blood  should 
be  injected  intraperitoneally  in  a  mouse.  General 
septicemia  will  follow. 

PUERPERAL   INFECTION. 

1.  Blood  cultures  will  show  streptococci  and  staphy- 
lococci. 

2.  "Doderlein's  cultures"  from  the  uterus  should  also  be 
made. 

SCARLET  FEVER. 

1.  Especially  in  severe  and  complicated  cases  strepto- 
cocci may  be  found  in  the  blood. 


THE  MALARIAL  PARASITES. 

PLASMODIUM  VI VAX  is  associated  with  the  tertian  form  of 
intermittent  fever  in  which  the  paroxysms  occur  every 
48  hours. 

PLASMODIUM  MALARI/E  is  associated  with  the  quartan 
form  of  intermittent  fever  in  which  the  paroxysms  occur 
every  72  hours, 

PLASMODIUM  FALCIPARUM  is  associated  with  estivo- 
autumnal  fever.  Duration  of  cycle  segmentation  varies 
from  24  to  72  hours. 

Note. — The  parasites  are  recognizable  in  both  the  un- 
stained and  in  stained  smears.  For  staining,  the  thionin, 
Nocht  and  Wright  stains  are  preferred.  The  parasites 
are  easily  recognized  in  the  unstained  smears. 

TERTIAN   PARASITE   UNSTAINED. 

YOUNGEST    (OR    HYALINE)    FORMS   appear   as 

Small    (2    microns),    colorless,    non-pigmented    disc. 

57 


This   shows   an  undulating    rim    of    protoplasm, 
which  encloses  a  single  large  nuclear  body. 

This  body  is  surrounded  by  a  ''milky  zone." 
It  is  actively  ameboid  and  changes  its  shape  and 
position. 

WHEN   12  HOURS  OLD. 

Ameboid  motion  very  active  so  that  pseudopodia 
may  be  seen  which  are  very  refractile. 

Pigment  now  appears  in  the  parasite. 

They  are  light-brown  granules  with  a  rapid  danc- 
ing motion. 

These  granules  seem  to  be  especially  gathered  in 
the  ends  of  the  pseudopodia. 

Size:    increases  and  also  the  R.  B.  C. 

WHEN   24   HOURS   OLD. 

Size:    fills  about  Vs  of  the  R.  B.  C. 
Still  actively  ameboid. 
Pigment  increased. 

Pigment  is   darker. 

Less  actively  motile. 

Scattered  all  over  the  parasite. 

AT  40  HOURS  THE  PARASITE  IS  FULLY  DEVELOPED. 

Size:    8  to  10  microns. 

Shape:    round.     Less  distinct  than  the  red  cell. 
Pigment:    more  abundant  and  evenly  distributed. 
The  R.  B.  C.  at  this  stage. 

Is  about  IVz  times  its  normal  size. 

Its  outline  can  hardly  be  recognized. 

PRESEGMENTAL  STAGE. 

Pigment:     collects  in  the  form  of  irregular  clumps, 
the  granules  moving  in  irregular  lines. 

Outline:    periphery  of  parasite  slightly  crenated  and 
refractive  dots  appear  on  its  border. 

R.  B.  C:    disappears  and  the  parasite  becomes  more 
dense  and  highly  refractile. 

58 


SEGMENTAL   STAGE. 

Striations:  from  the  crenated  border  radial  lines  ap- 
pear in  so-called  "rosette"  or  "daisy-head"  form. 
These  radii  are  directed  toward  the  center  of  the 
parasite  and  between  these  divisions  we  see 
highly  refractile  dots. 

The  segments  become  more  and  more  distinct. 

They  finally  separate  into  circular  bodies  hav- 
ing a  central  refractile  dot. 

Pigment:  irregularly  scattered  between  these  seg- 
ments. (Each  segment  is  a  hyaline  form  ready 
to  attack  another  R,  B.  C.) 

Besides  the  above-described  intracellular  hyalines,  'we 
occasionally  find  extracellular  forms  of  the  tertian  parasite. 
There  are  two  varieties. 

(a)  DEGENERATIVE  FORMS. 

These  are  extruded  intracellulars  which  have 
died. 

If  it  leaves  the  cell,  the  Hb.  passes  out  of  the  cell, 
leaving  a  corpuscular  shadow. 

But  this  does  not  always  occur,  so  that  we 
usually  find  "dumbbell-shaped"  organisms  in  the 
plasma. 

During  extrusion,  the  pigment  is  in  active  mo- 
tion but  ceases  as  the  parasite  dies. 

Sometimes  the  parasite  breaks  up  into  frag- 
ments forming  pigmented  spherical  bodies. 

Or,  they  may  be  deformed  and  vacuolated — they 
are  then  called  ''sporulating  forms." 

(b)  GAMETOCYTES. 

Usually  present  in  the  blood  a  few   days  after 
the   Infection  sets  in. 
There  are  2  forms 

1.  Female  or  macrogamete. 

2.  Male  or  micrcgamete. 

1.     Female  or  macrogamete. 

Three  or  four  times  the  size  of  a  red  cell. 
Pale,  indistinct  but  actively  ameboid. 
Abundant  pigment. 
Some  show  no  trace  of  the  R.  B.  C. 
Nucleus  is  31/2  microns  and  is  sometimes  seen 
in  the  fresh  specimen. 

59 


It  is  recognized  by  the  fact  that  it  is  the 
only  portion  of  the  parasite  which  is  not  in- 
maded  by  the  pigment  granules. 

The  female  is  formed  from  a  flagellum  of  the 
parent  cells,  the  microgametocyte. 

The  microgametocyte  or  parent  cell  is 

Smaller  than  its   offspring    (female)    be- 
ing only  8   to   10   microns   in  diameter. 

Its   pigment   is   at  first  active.     It   soon 

forms  a  circle  around  the  center  and  becomes 

motionless. 

Sometimes  it  pushes  out  several  flagella 

which  are  the  microgametes. 
2,     Male  or  microgamete. 

Two  or  3  times  the  size  of  a  R.  B.  C. 

Often  contains  pigment  granules. 

These  flagella  break  away  from  the  parent 
cell,  the  latter  then  appearing  as  a  small  cell 
with  central  motionless  pigment. 

Flagellation  does  not  occur  in  fresh  speci- 
mens but  occurs  15  to  20  minutes  after  the  blood 
is  drawn. 

QUARTAN    PARASITE    UNSTAINED. 

EARLY  HYALINE  FORMS  cannot  be  differentiated  from 
tertian  but  are  easily  recognized  when  pigment  ap- 
pears. 

Pigment  is  coarser,   darker  in  color,  not  so  actively 
motile. 

AS  THE   PARASITE  GROWS— 

Protoplasm:    highly  retractile. 

Pseudopodia:     very  distinct. 

Motility:    less  active. 

R.  B.  C. :     become  smaller;   margins  crenated. 

WHEN  24  HOURS  OLD. 

Shape:     round  or  oval  and   very  distinct. 
Slightly  ameboid. 
Pigment:    blackish-brown. 

Peripheral   location   especially   on  one   side. 

Not  motile  at  this  stage. 

(In  the  tertian  the  pigment  is  scattered  all  over.) 
R.  B.  C:     very  small,  crenated,  brassy  in  color. 

60 


AS   IT  CONTINUES  TO   GROW— 

It  becomes  rounder  and  motility  ceases. 
Protoplasm  very  distinct  and  highly  refractile 
Fills   1/3  to   1/2   of  the  R.  B.  C. 

DURING   THE   THIRD   DAY. 

^"  ^brass  ^""^^  ^  ^^^  '^  ^^"'  ^^^  '^'^  '^  ^^""^  ^^*^ 
The  parasite  is  full  grown  (7  microns). 
Pigment:  travels  from  the  periphery  to  the  center 
in  definite  radial  lines  like  the  spokes  of  a  whe^l 
the  pigment  granules  forming  the  spokes.  But 
the  pigment  soon  collects  in  the  center  This  is 
the  presegmenter  form. 

The  parasite  now  becomes  opaque  and  "rosette"  de- 
marcations appear.  There  are  6  to  12  segments. 
These  segments  are  more  perfect  than  the  tertian' 

they  become  detached  as  hyaline  forms  and  are  ready 

to  attack  red  cells  again. 
Gamete  forms:     Rarely  seen  here. 

Resemble  the  tertain  but  usually  smaller. 

ESTIVO-AUTUMNAL  PARASITE  UNSTAINED. 
HYALINE    FORMS. 

Resemble   the   other  forms   but  slightly   smaller 

pearance'mth''ltrer.""'"  '°  '°™  '""'  ■■^'^'"  *-  ^P" 
ceUs'toSk.)™"  "^'  '"'■""^  '"  "^^'  "  ^^"-^  «^«  ^^a 
.in.i','  *^""""''   "'°™   '""   quartan   by   its   smaller   dimen- 

Those  rings  which  do  not  show  the  signet-ring  ap- 
pearance always  present  2  nuclear  bodies  lying  at  opposite 
poles  or  close  together.  ^       opposite 

AS  THE   PARASITE    DEVELOPS. 

Pigment:  slight  amount  appears;  usually  motionless- 
located  at  periphery  or  at  inner  edge  of  the  bi- 
concavity. 

Size:    occupies  1/5  of  cell. 

R.  B.  C:  exceedingly  shrunken,  crenated  and  brassy 
even  m  the  early  stages.     The  infected  R.  B.  C. 

61 


now    disappear    from    the    peripheral    circulation 
and  migrate  to  the  lymph  glands,  especially  the 
spleen,  there  to  continue  its  development. 
Blood  from  a  splenic  puncture  will  show: 

Pigment:    greatly  increased,  coarser  and  darker, 
thus  greatly  resembling  the  quartan. 

Size:    parasite  increased  to  5  microns. 

When   full    grown   its   pigment  is   in   the   center. 

(Never  diffuse  as  in  the  tertian.) 
(More  peripherally  located  than  in  the  quartan.) 
Rarely  seen  in  peripheral  circulation. 
Segmentation.     Similar  to  other  forms. 

Usually  15  very  small  segments. 

SEVENTH    DAY    OF  THE    DISEASE    (in   the    peripheral 
blood). 

CRESCENTS  AND  OVOIDS  APPEAR. 
CRESCENTS. 

Crescentic  in  shape  with  rounded  ends. 

Slightly  longer  than  a  R.  B.  C. 

Very  retractile. 

Pigment  in  center. 

Granules  usually  coarse  and  rod-shaped. 

The  crescents  frequently  change  their  shape 
to  oval,  dumbbell,  circular  and  then  re- 
sume the  original  form. 

A  small  portion  of  the  degenerated  R.  B.  C. 
is  attached  to  the  crescent. 

OVOIDS      Have  no  corpuscular  remnant. 
Protoplasm  not  so  refractile. 

TERTIAN   PARASITE  STAINED. 

YOUNG   HYALINE   FORMS  of  the  parasite. 
Protoplasm:    ring-shaped,  stained  blue. 

Achromatic  area:  a  colorless  "milky"  area  enclosed 
in  the  protoplasm. 

Nucleus:  a  reddish-violet  punctate  spot  at  the  thin- 
nest portion  of  the  ring  which  is  shaped  like  a 
"signet-ring." 

Size:    2  to  3  microns. 

Location:    in  the  center  of  a  R.  B.  C. 

Non-pigmented. 

62 


A   PARASITE   24    HOURS   OLD. 

"Milky  area"  increases  in  size. 

Chromatin  dot  begins  to  break  up  into  groups  of 
nuclei. 

Pigment  appears  in  the  form  of  fine  grains. 

R.  B.  C.  grow  larger  and  paler. 

MATURED  OR  FULL  GROWN   PARASITE. 

Chromatin:  completely  broken  up  and  diffusely  scat- 
tered over  the  R.  B.  C.  in  the  form  of  strands  or 
masses. 

These  chromatin  clumps  divide  into  15  to  20 
dense  round  masses. 

Around   these   masses   protoplasm   begins   to 
collect. 

In   this    stage,    the    protoplasm   is    devoid    of 
color  and  it  is  always  so  in  the  segmenting  cell. 

Each  of  these  chromatin  clumps  has  a  milky 
zone. 

Pigment:    greatly  increased. 

Size:  at  48  hours  the  parasite  occupies  almost  the 
entire  swollen  R.  B.  C. 

Segmentation:    occurs  between  40  and  48  hours. 

Pigment:     collects  centrally  "en  masse." 

Protoplasm:    divides  in  rosette  or  "daisy-head." 

Note. — Some  full-grown  tertian  parasites   do   not 
divide  into  segments. 

These    forms    contain    actively    dancing    pigment 
granules  in  the  unstained  specimen.      (See  p.  58. j 

QUARTAN  PARASITE  STAINED.  Resembles  tertian  para- 
sites but 

Chromatin  mass  is  indistinct  in  the  hyaline  forms  and 
in  the  older  forms  appears  as  an  irregular  clump  of 
granules. 

As  it  continues  to  grow,  the  parasite  takes  a  form 
extending  across  the  cell  and  occupies  the  major  portion 
of  the  R.  B.  C.  which  has  become  shrunken  and  irregular 
in  shape. 

SEGMENT   FORMS  are  more  distinct. 

(a)     They    show    more    regular    and    geometric    lines    of 

cleavage  with  the  chromatin  exactly  in  the  center 

of  the  crenated  surface. 

63 


(b)     The  pigment  granules  are  coarser  and  much,  more 
distinct  and  more  peripherally  located. 

Note. — Some  full-grown  parasites  do  not  segment. 

ESTIVO-AUTUMNAL   PARASITE   STAINED. 
HYALINE   FORMS. 

Chromatin:    appears  as  2  or  more  dots  or  filaments. 

Protoplasm:  scantier  than  in  the  other  forms.  Thick- 
ening of  the  protoplasmic  layer  opposite  the 
chromatin  mass  is  very  diagnostic. 

GAMETE  FORMS.     Are  distinctly  spherical,  being  of  the 
same  thickness  all  the  way  round. 

Nucleus  forms  a  portion  of  the  ring  but  does  not  pro- 
ject as  in  the  asexual  parasites.  The  R.  B.  C.  in 
these  sexual  types  do  not  show  any  coarse  granu- 
lar stippling. 

CRESCENT    FORMS.      Very   diagnostic    of   this    form    of 
malaria. 

(a)      Male  crescent. 

Chromatin:    occupies   the   major   portion   of  the 
cell.     Appears  as  a  loose  net-work. 

Protoplasm:    little  and  stains  blue. 

Pigment:     universallj^   scattered   throughout   its 
body. 

Shape :    somewhat  kidney-shaped  and  shorter  and 
broader  than  the  female, 
fb)      Female  crescent. 

Size:    larger  and  narrower  than  male. 
Chromatin:    compact  and  centrally  located. 
Pigment:    in  a  ring  around  the  nucleus  or  in  a 
clump  at  the  center. 

Protoplasm:    abundant  and  bluish  in  color. 

CIRCULAR  FORMS.     Two  types  are  present: 
1.     Microgametocyte. 

Size:    smaller  than  a  R.  B.  C. 
Shape:    distinctly  spherical. 

Chromatin:    in  center  in  a  large  irregular  mass  or 

in  several  dense  masses  near  the  periphery. 

These   masses   containing   chromatin   are 

later   extruded   and   form   the   flagella   or   mi- 

crogametes. 

64 


2.     Macrogametocyte. 

Size:    2  or  3  times  the  former. 
Shape:    often  triangular. 
Protoplasm:    abundant  and  blue-staining. 
Chromatin:    in  a  single  mass  at  the  periphery  and 
is  surrounded  by  a  circle  of  pigment. 


THE  MALARIAL  FEVERS. 

1.  For  description  of  the  parasites,   see  pages  57  to  64. 

2.  Enormous  reduction  in  the  number  of  R.  B.  C.  occurs 
in  acute  attacks.  A  count  of  one  million  may  be  ob- 
tained on  the  first  day. 

3.  In  chronic  cases  we  find  features  of  a  secondary 
anemia. 

Polychromatophilia  and  granular  degeneration  of 
the  R.  B.  C.  progress  steadily. 

The  estivo-autumnal  parasite  may  create  a  blood 
picture  closely  resembling  that  of  pernicious  anemia. 

The  quartan  and  estivo-autumnal  parasites  cause 
a  shrinking  of  the  R.  B.  C.  and  these  cells  assume  a 
brassy  tone. 

4.  Absence  of  leucocytosis.  But,  relative  lymphocytosis 
just  as  in  typhoid. 

5.  In  the  afebrile  period  and  sometimes  throughout  the 
disease  eosinophilia  occurs. 

6.  Pigmented  leucocytes  very  common.     (Phagocytes.) 

RELAPSING   FEVER. 

1.  In  fresh  blood,  actively  motile,  cork-screw  organisms 
are  readily  seen. 

2.  A  dried  smear  stained  with  fuchsin  or  the  aniline 
dyes  depicts  the  Spirochetae  of  Obermeier  plainly. 

3.  The  spirilli  can  only  be  found  during  the  febrile 
paroxysm.  In  the  fresh  specimen  it  is  seen  to  move 
slowly  among  the  R.  B.  C.  but  does  not  molest  them. 

4.  With  each  successive  paroxysm  the  spirilli  increase  in 
number. 


65 


5.  A  leucocytosis  is  very  characteristic  of  this  disease, 
especially  just  after  the  crisis.  The  disease  is  also 
called  "Seven-day  Fever." 

TRYPANOSOMIASIS.     (SLEEPING  SICKNESS.) 

1.  A  nucleated,  fusiform,  flagellated  parasite,  the  trypan- 
osoma  Gambiense,  having  an  undulating  membrane 
may  be  seen  in  the  blood  but  never  within  the  cor- 
puscles. 

2.  The  parasites  vary  greatly  in  number  from  day  to 
day. 

3.  Best  stained  with  the  polychrome  dyes.     They  show — 

(a)  nucleus,  which  is  large  and  red. 

(b)  Centersome,  intensely  stained  and  located  in  a 
vacuole-like  area  near  the  blunt  end. 

(c)  Line  of  chromatin  running  down  the  edge  of  the 
undulating  membrane  and  terminating  in  the 
flagellum.  The  chromatic  line  and  flagellum  are 
both  stained  red. 

(d)  Protoplasm  of  the  body  is  distinctly  blue. 

4.  In  genuine  cases,  the  parasites  should  be  found  in 
the  cerebro-spinal  fluid. 

FILARIASIS. 

1.  The  filaria  sanguinis  hominis  (Bancrofti)  are  seen 
under  the  microscope  in  active  motion.  However,  they 
lose  their  motility  very  quickly. 

2.  The  embryo  is  surrounded  by  a  sheath  which  is  con- 
siderably larger  than  the  parasite  and  shows  fine  cross 
striations. 

3.  They  are  about  the  thickness  of  a  red  cell  and  about 
l/90th  of  an  inch  long. 

4.  All  examinations  must  be  made  at  night,  their  num- 
bers gradually  rising  to  a  maximum  about  midnight. 

5.  Only  the  embryos  are  found  in  the  blood;  the  adult 
forms  remaining  in  the  lymphatics  where  they  ob- 
struct the  flow  of  lymph  and  cause  lymph-scrotum, 
hematochyluria,  etc. 

6.  A  thick  blood  smear  is  essential. 

7.  Eosinophilia  is  very  characteristic. 

66 


SYPHILIS. 

1.  The  spirochaete  pallida  can  be  demonstrated  in  both 
peripheral  blood  and  in  the  blood  from  a  splenic  punc- 
ture and  in  certain  skin  lesions  when  a  dark  field  il- 
luminator is  used. 

2.  Best  stained  with  Goldhorn's  stain. 

Technic. 

1.  Fix    smear   with    pure   methyl   alcohol   for    1.5 
minutes. 

2.  Flood   with   polychrome   methylene   blue   3   to 


seconds. 


3.  Drain  the  excess  off. 

4.  Place  slide  slowly  in  clean  water  (film  side 
down)  and  keep  in  this  position  5  seconds. 

5.  Shake  in  water  to  remove  excess  of  the  dye. 
The  spirochaete  appear  violet  colored. 

6.  By  staining  with  Gram's  iodine  solution  for  15 
to  20  seconds,  washed  and  dried,  and  examined 
with  oil-immersion  lens,  the  organisms  give 
up  their  violet  color  and  become  bluish-black. 

3.     Other  good  stains  are:    Giemsa's  and  Levaditi's. 

ROCKY  MOUNTAIN  SPOTTED  FEVER.     (Tick  fever.) 

1.  The  parasite,  the  piroplasma  hominis  attacks  the  red 
cells. 

2.  Three  forms  of  this  intracellular  ovoid  parasites  occur. 

3.  Best  stained  with  polychrome  dyes. 

TEST  FOR  PUS  IN  THE  BLOOD.    (lODOPHILIC  REACTION.) 

1.  A  dried  unfixed  blood  smear  is  first  exposed  to  the 
vapors  of  solid  iodine  until  it  assumes  a  brownish 
color. 

2.  Then  mount  with  this  titration: 

Iodine 1  G. 

Potassium   iodide 3  G. 

Dist.  water 100  c.c. 

To   which   a   sufficient   amount   of  gum   arable   is 
added  to  make  a  syrup  (a  brownish,  ropy  fluid). 

3.  One  drop  of  this  titration  is  sufficient.  The  cover 
slip  should  be  pressed  tightly. 

4.  After  15  minutes  examine  with  oil-immersion  lens. 

67 


Positive   reaction. 

Brown  or  mahogany  colored  granules  within  the  poly- 
morphonuclear leucocytes.  The  protoplasm  may  also  at 
times  show  a  diffuse  brown  stain. 

Although  the  reaction  is  usually  confined  to  the  neu- 
trophiles,  the  mononuclear  cells  may  also  be  tinged  brown. 

This  so-called  intracellular  reaction  is  more  important 
than  the  extracellular  reaction  in  the  blood  plates. 

Negative  reaction. 

In  the  absence  of  pus,  the  protoplasm  of  the  leucocytes 
are  stained  bright  yellow  and  the  nuclei  are  much  lighter. 

BREMER'S  BLOOD  TEST  IN  DIABETES. 

1.  A  thick  fresh  blood  smear  is  fixed  by  dry  heat  and  al- 
lowed to  cool. 

2.  Then  flood  with  a  1%  aqueous  solution  of  congo-red 
for  a  few  minutes. 

3.  Wash  in  water. 

Normal   blood:    stains  bright  red. 

Diabetic  blood:    either  refuses  to  stain  or  else  takes  on  a 

faint  yellowish  or  greenish  hue. 

May  be  obtained  before  glycosuria  becomes  marked. 

A  positive  reaction  may  occur  in  other  diseases,  e.  g., 
leukemia,  goitre,  Hodgkin's  disease,  etc.,  hence  it  is  not 
a  specific  test. 

Note. — A  1%  solution  of  Biebrich  Scarlet  will  stain 
diabetic  blood  intensely,  whereas  normal  blood  does  not 
take  up  the  stain. 

In  diabetes,  the  blood  shows  lipemia.  Extracellular 
fat  globules  are  seen. 

WILLIAMSON'S  TEST   IN    DIABETES. 

1.  Dissolve  2  drops  of  blood  in  4  drops  of  water. 

2.  Then  add  1  c.c.  of  a  1:6,000  aqueous  solution  of 
methylene  blue. 

3.  To  this  add  4  drops  of  a  6%  solution  of  liquor  potassae. 

4.  The  test  should  be  performed  in  a  test  tube.  At  this 
point  place  the  test  tube  in  boiling  water  for  4  minutes. 
Normal  blood:    color  remains  deep  blue. 

Diabetic  blood:    decolorizes  the  solution. 
Diabetic  urine:    gives  same  reaction. 

Note. — Do  not  use  more  blood  than  what  is  stated 
above  because  decolorization  will  occur  with  larger 
quantities. 

68 


GRUBER-WIDAL   REACTION    IN  TYPHOID. 

THE  "HANGING-DROP"  OR   MICROSCOPIC  METHOD. 

1.  With  a  special  capillary  pipette  with  a  central 
bulbar  enlargement,  draw  up  15  to  20  drops  of 
blood  from  a  pricked  ear. 

2.  Lay  the  pipette  fiat  until  coagulation  occurs.  The 
serum  which  exudes  is  preferable  to  whole  blood. 

3.  Serum  may  also  be  obtained  by  using  cantharides 
so  as  to  cause  a  blister. 

4.  Dilute  this  serum  with  physiological  salt  solution 
(performing  this  on  watch  crystal)  so  as  to  make 
one  dilution  of  1:25  and  another  one  of  1:50. 
(This  means  one  drop  of  serum  and  24  and  49 
drops  of  salt  solution.) 

5.  Take  one  platinum  loop  full  of  each  dilution  and 
mix  with  one  loop  of  a  standard  suspension  of 
typhoid  germs.  The  dilutions  are  now  1:50  and 
1:100.  These  typhoid  suspensions  must  be  fresh 
and  the  germs  must  be  actively  motile.  Strains 
which  have  passed  through  several  generations 
on  artificial  media  are  the  best. 

6.  From  the  above  last  2  dilutions,  hanging-drop  prep- 
arations should  be  made  and  examined. 

Reaction.  With  a  dilution  of  1:50,  and  within 
a  period  of  one  hour,  a  marked  clumping  together 
and  complete  loss  of  motility  of  these  typhoid 
germs  signifies  a  positive  reaction.  THE  TIME 
and  DILUTION  ARE  VERY  IMPORTANT. 

MACROSCOPIC  METHODS.  Cultures  which  have  been  killed 
by  heat,  formalin,  carbolic,  etc.,  are  employed.  Clumps 
of  bacilli  settle  to  the  bottom  of  the  test  tube  leaving  a 
clear  supernatent  liquid.  Picker's  Typhus  Diagnostikum 
very  good.    It  is  sold  by  Merck  &  Co. 

BASS    AND    WATKIN'S    MODIFICATION    OF    THE    MACRO- 
SCOPIC METHOD. 

1.  Mix  a  full  drop  of  blood  serum  with  4  drops  water. 

2.  Add  4  drops  of  the  following  suspension  to  the  above. 
(10,000  million  killed  typhoid  germs  per  c.c.  in  1.7% 
NaCl  to  which  1%   formaline  is  added.) 

3.  Tilt  slide  from  side  to  side  so  as  to  keep  the  mixture 
flowing  back  and  forth. 

69 


Positive  reaction.  Grayish,  mealy  sediment  within  one 
minute.  This  sediment  appears  in  the  fluid  and  around 
the  edges  and  tends  to  collect  there.  If  the  agitation 
he  continued,  the  clumps  increase  in  size  for  2  or  3 
minutes. 

Negative  reaction.  Absence  of  agglutination  of  the  mix- 
ture. It  remains  clear.  If  the  reaction  fails  to  ap- 
pear within  2  or  3  minutes  it  will  not  appear  at  all. 

Advantage.     Can  be  quickly  performed  at  bedside. 
Reliability. 


BLOOD  TESTS  FOR  SYPHILIS. 

1.     JUSTUS'S  TEST. 
A  rapid  reduction  in  the  percentage  hemoglobin    (10   to 
20%)  follows  mercurial  treatment  (inunction  or  injection)   in 
florid  syphilitic  patients.     It  lasts  from  a  few  hours  to  a  few 
days. 

Objection.  Mercury  salts  alone  may  cause  an  anemia  in 
consequence  of  their  hemolytic  action  upon  the  red  blood  cor- 
puscles. 

2.     SERUM  COLOR  REACTIONS. 

1.  To  0.1  c.c.  serum  add  enough  physiological  salt   solution 
to  bring  the  quantity  up  to  3  or  4  c.c. 

2.  Then  add  1  drop  perhydrol  (as  an  oxidizer). 

3.  Mix  this  with  0.5  c.c.  of  SchUrman's    reagent     (prepared 
fresh) : 

Carbolic  acid 0.5 

5%  aqueous  solution  ferric  chloride 0.62 

Distilled  water 34.5 

Positive  reaction.  As  the  reagent  is  allowed  to  trickle 
down  the  test  tube,  a  dark  brown  color  will  be  ob- 
served at  the  junction  of  the  fluids.  On  shaking,  the 
mixture  appears  very  thick.  To  be  of  value,  the  re- 
action must  occur  within  1  or  2  minutes. 

Normal  blood  serum.  A  slight  green  ring  occurs  at  the 
junction  of  the  liquids.  But,  it  disappears  almost  en- 
tirely on  shaking.  The  mixture  also  remains  clear 
and  transparent. 

Note. — Landau's  serum  color  reaction  is  now  in  its 
experimental  stage.  Reports  thus  far  do  not  affirm  its 
specificity  for   syphilis. 

70 


3.      WASSERMANN'S  REACTION. 

1.  The  Wassermann  test  or  any  of  its  modifications,  when 
positive,  is  a  specific  test  for  lues. 

A  negative  reaction  does  not  rule  out  syphilis. 

Repeated  examinations  are  necessary. 

2.  The  Noguchi  modification  is  superior  to  the  Wassermann 
test  because  the  percentage  of  positive  results  is  some- 
what higher. 

3.  Under  vigorous  mercurial  treatment  and  with  "696"  a 
positive  test  once  obtained  may  disappear,  but  it  does  not 
mean  that  the  patient  is  cured. 

4.  All  tests  are  based  on  the  Bordet-Gengou  phenomenon  of 
complement  fixation  to  determine  the  presence  of  the 
syphilitic  antibody  in  the  patient's  blood  serum.  The  tests 
are  interpreted  according  to  the  degree  of  hemolysis  visible 
in  the  test  tubes. 


THE  A-B-C  OF  THE  SERUM  DIAGNOSIS  OF 

SYPHILIS. 

DEFINITION    OF    TERMS. 

HEMOLYSIS.  Dissolution  of  the  red  blood  corpuscles  and 
the  passing  out  of  the  red  coloring  matter  (hemoglobinj 
into  any  medium  in  which  the  erythrocytes  may  be  sus- 
pended. 

Hemolytic    substances    are    those    substances    capable    of 
producing  hemolysis.      (See  page   51.) 

Fresh   blood   of  many   animals   is   hemolytic    for   the 
R.  B.  C.  of  some,  but  not  all,  other  species. 

Hemolysis  depends  upon  three  factors: 
1.    Amboceptor. 


2.  Complement. 

3.  Corpuscles. 


Amboceptor   cannot  act  without 
complement. 

Complement  cannot  act  without 
amboceptor. 

Both  combined  must  act  on  the 
R.  B.  C. 

71 


COMPLEMENT. 

1,  It  is  one  of  the  factors  necessary  for  hemolysis. 

2.  It  is  always  present  in  fresh  sera. 

3.  It  is  destroyed  by  heating  for  one-half  hour  at  55°  C. 
Serum  thus  heated  becomes  inactivated. 

4,  If  the  serum  be  taken  from  a  guinea-pig,  it  is  called 
guinea-pig  complement. 

Inactivation.     Depriving  fresh  serum  of  its  complement. 
Reactivation. 

1.  When    fresh    serum    is    added    to    an    inactivated 
serum  the  latter  again  becomes  activated. 

2.  Complement  can  always  reactivate  the  serum  of 
the  same   species  from  which  it  is  derived. 

But,  not  every  complement  can  activate  the 
sera  of  other  species.  However,  guinea-pig  com- 
plement is  characterized  by  its  remarkable  ability 
to  reactivate  sera  of  alien  species.  It  is,  there- 
fore, used  whenever  it  becomes  necessary  to  sub- 
stitute the  complement  of  one  serum  for  that  of 
another  which  has  become  inactivated  or  has  de- 
teriorated. 

AMBOCEPTOR  OR   HEMOLYSIN. 

1.  The  serum  of  the  blood  of  an  animal  which  has  been 
immunized  with  R.  B.  C.  of  another  species  gives  us 
amboceptor.  The  injected  animal  develops  in  its 
serum  anti-bodies. 

2.  It  is  one  of  the  three  factors  necessary  for  the  pro- 
duction of  hemolysis. 

3.  It  is  stable;  not  being  destroyed  by  heating  as  is  the 
case  with  complement. 

4.  Amboceptors  are  specific.  They  can  act  upon  the 
R.  B.  C.  of  one  animal  only.  The  prefix  "anti"  is 
usually  added  to  the  name  of  the  species  which  has 
been  used  to  bring  about  the  immunization. 

5.  Some  sera  contain  several  kinds  of  amboceptors.  Thus 
one  particular  serum  may  have  amboceptors  for  sheep, 
for  rabbits,  for  dogs,  etc. 

6.  Natural  amboceptors.  Are  those  amboceptors  already 
existing  in  the  serum  of  a  given  animal. 

72 


7.  Immune  amboceptors.  By  repeatedly  injecting  an  ani- 
mal with  R.  B.  C.  of  another  alien  animal,  we  may 
create  specific  amboceptors  for  this  animal,  or,  we 
may  increase  the  amount  of  natural  amboceptor  al- 
ready present. 

When  red  blood  cells  are  injected,  the  amboceptors 
created  are  also  designated  as  hemolytic  amboceptors 
for  the  purpose  of  contrasting  to  bacteriolytic  ambo- 
ceptors which  are  produced  when  bacteria  are  in- 
jected into  an  animal.  The  dissolution  of  the  bacteria 
(whereas  in  the  other  case  it  is  the  corpuscles)  is 
known  as  bacteriolysis  as  compared  to  hemolysis. 

After  immunization,  the  serum  of  the  immunized 
animal  gradually  loses  its  hemolytic  power,  but  may 
be  rapidly  increased  by  a  few  injections  of  the  red 
cells  first  used  in  the  process  of  immunization. 

ANTIGENS. 

1.  A  general  term  applied  to  a  group  of  substances  cap- 
able of  producing  specific  antibodies  (w^hen  injected 
into  a  suitable  animal).  Diphtheria  toxin  is  an  antigen 
because  injections  thereof  are  followed  by  the  ap- 
pearance of  a  specific  antitoxin  in  the  horse.  Red 
blood  cells  and  bacteria  may  also  act  as  antigens. 

2.  These  antibodies  are  specific  for  the  substances  from 
whence  they  are  derived.  Given  a  known  antibody  we 
can  determine  the  unknown  antigen  owing  to  this 
specificity. 

COMPLEMENT    FIXATION. 

1.  A  disappearance  of  the  complement  in  a  mixture  of 
antigen  and  antibody. 

2.  A  distinct. relation  exists  between  the  combination  of 
antigen  and  antibody  with  that  of  complement. 

The  R.  B.  C.  (as  antigen)  acted  upon  by  ambo- 
ceptor (antibody)  becomes  so  altered  as  to  absorb 
the  comxplement  and  undergo  hemolysis. 

In  the  same  way,  bacteria  as  antigen,  having  been 
acted  upon  by  amboceptor  (antibody),  take  up  the 
complement  and  become  dissolved. 

3.  Sera  of  various  animals  show  marked  differences  in 
their  power  of  complement  fixation. 

73 


4.  Whereas  a  given  serum  might  possess  the  property 
of  reactivating  the  hemolytic  amboceptor  of  an  in- 
activated serum,  tliis  same  serum  of  tlie  given  species 
may  possess  little  or  no  fixation  property.  This  fact 
is  very  useful  in  diagnosis. 

Guinea-pig's  complement  is  very  readily  fixed. 

Rabbit's  complement  possesses  the  best  reactivat- 
ing property  for  the  rabbit's  amboceptor. 

5.  By  means  of  the  complement  fixation  reaction,  antigen 
may  be  detected  indirectly.  Antigen  may  also  be  de- 
tected directly  because  of  the  specificity  of  antibody 
and  antigen. 

6.  Five  factors  enter  into  the  complement  fixation  reac- 
tion in  the  diagnosis  of  syphilis. 

i.     Red  blood  cells. 

ii.     Hemolytic  amboceptor. 

iii.     Complement. 

These  three  are  collectively  designated  as 
the  ''hemolytic  system." 

iv.     Syphilitic  antigen  or  extract  of  syphilitic  liver. 
Whereas  the  R.  B.  C.  are  also  antigens,  we 
do  not  refer  to  these  antigens  vv^hen  the  term 
antigen  is  used,  but  to  syphilitic  antigen. 

V.  Antibody.  Whereas  hemolytic  amboceptor  is 
also  an  antibody,  antigen  as  used  in  the  test, 
refers  to  antibody  present  or  absent  in  the 
serum   under  investigation  for   syphilis. 

ANThCOMPLEMENTARY    SUBSTANCES    AND    ANTI-COM- 
PLEMENTARY ACTION. 

Substances  possessing  the  power  of  reducing  or  totally 
removing  the  action  of  the  complement  are  designated 
as  anti-complementary. 

Most  acids,  alkalies  and  certain  salts  have  such  action. 

Such  substances  may  also  be  present  in  certain  sera. 
Human  serum  gradually  acquires  this  property  on  stand- 
ing. Repeated  injections  of  fresh  serum  into  an  animal 
of  another  species  causes  the  production  of  such  sub- 
stances. (Ehrlich  and  Morgenroth).  Bacterial  infection 
may  cause  the  serum  to  become  anti-complementary  but 
it  is  said  that  heating  to  56°  C.  for  30  minutes  rids  the 
serum  of  this  difficulty. 

74 


BASIS  OF  THE  WASSERMANN   REACTION  AND  ITS  MODI- 
FICATIONS. 

The  complement,  which  is  essential  for  the  production 
of  hemolysis  (dissolution  of  the  red  cells)  is  fixed  so  that 
it  cannot  take  part  in  this  process.  The  result  is  that  no 
hemolysis  can  take  place.  Inhibition  of  hemolysis  is  not 
necessarily  complete.  Our  conclusions  are  based  upon 
the  degree  or  extent  of  the  inhibition  of  hemolysis.  The 
results  are  expressed  in  percentages  or  by  a  variable 
number  of  plus    (  +  )    signs. 


1.     The  Original  Wassermann  Test. 

1.     ANTIGEN.     A  watery  extract  is  used  in  the  original  test. 

(a)  The  liver  or  spleen  of  a  congenitally  syphilitic 
fetus  is  cut  up  into  small  pieces  and  minced  in 
a  meat  grinder. 

(b)  For  every  part  of  tissue  add  4  parts  normal  salt 
solution  to  which  carbolic  acid  is  added  in  the 
proportion  of  O.o7c. 

(c)  Shake  the  mixture  well  in  a  dark  bottle  for  24 
hours  by  means  of  a  shaking  machine. 

(d)  Centrifuge.  The  brownish  opalescent  super- 
natent  liquid  is  antigen.  It  must  be  preserved 
m  a  rubber-stoppered  brown  bottle  in  a  refrip-- 
erator,  ^ 

On  standing,  a  precipitate  sediments.  This 
should  neither  be  used  nor  disturbed.  When  in 
need  of  antigen,  decant  the  required  amount  of 
antigen  and  replace  balance  in  refrigerator.  Do 
not  expose  to  light. 

(e)  Titration  of  antigen. 

Use  0.8,  0.6,  0.4  and  0.2  c.c.  of  the  extract 
m  the  presence  of  1  c.c.  complement,  twice  the 
hemolytic  dose  of  the  amboceptor  and  1  c.c.  of 
5%  sheep's  corpuscles  for  its  anti-complementary 
properties,  and  in  the  same  quantities  plus  1  c.c. 
of  5%   sheep's  cells  for  its  hemolytic  qualities. 

If  the  antigen  be  not  hemolytic  in  0.4  and 
not  anti-complementary  in  0.4  according  to  the 
rule  of  Weil  and  Nakayama,  this  antigen  will 
be  employed  in  one-half  of  0.4  c.c.  (equals 
0.2  c.c). 

75 


2.  PATIENT'S   SERUM. 

Blood  is  obtained  from  a  vein.  It  is  permitted  to 
clot  and  the  serum  is  collected. 

Serum  is  inactivated  by  heating  to  56°  C.  for  30 
minutes. 

Inactivation  must  be  performed  within  12  hours. 
The  native  complement  is  thus  destroyed. 

If  cerebro-spinal  fluid  be  employed,  do  not  in- 
activate. 

The  test  doses  are  0,1  and  0,2  c,c. 

3.  COMPLEMENT. 

One  c,c,  of  guinea-pig's  serum  in  1:10  dilution. 
It  must  not  be  older  than  12  hours, 

4.  AMBOCEPTOR. 

Rabbits  are  immunized  against  sheep's  R,  B,  C, 
by  intraperitoneal  injections.  One  unit  of  ambocep- 
tor should  be  determined  by  titrating  against  1  c.c. 
of  5%  suspension  of  washed  R.  B.  C,  of  sheep,  using 
0,5  c,c,  of  the  above  diluted  complement.  In  the  actual 
test  use  2  units. 

5.  CORPUSCLE  SUSPENSION. 

One  c.c.  of  a  5%  suspension  of  washed  sheep's 
corpuscles.  Should  be  kept  on  ice  and  not  older  than 
24  hours. 

Sheep  blood  is  drawn  into  a  sterile  wide-mouthed 
bottle,  in  which  are  a  number  of  glass  beads,  and 
vigorously  shaken  immediately  so  as  to  defibrinate 
the  blood  and  prevent  clotting. 


76 


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77 


WASSERMANN  TEST  WITH   SIX  TUBES. 

1.  Arrange  6  tubes  in  pairs  as  shown  under  the  discus- 
sion of  the  Noguchi  modification  on  page  83. 

2.  In  No.  1  and  No.  2,  place  0.2  c.c.  of  the  Inactivated 
serum  of  a  known  syphilitic. 

3.  In  No.  3  and  No.  4,  place  0.2  c.c.  of  the  inactivated 
serum  from  the  patient  in  question. 

4.  In  No.  5  and  No.   6,  place  0.2  c.c.  of  the  inactivated 
serum  of  a  known  normal  person. 

5.  To  all  of  the   tubes   add   0.1   c.c.   of  fresh  guinea-pig 
complement. 

6.  To  the  tubes  in  the  front  row  (Nos.  1,  3  and  5),  add 
one  unit  antigen. 

7.  To  all  of  the  tubes  add   3   c.c.  normal  salt  solution. 

8.  Shake  all  tubes  vigorously. 

9.  Incubate  at  37°   C.  for  one  hour  and  then  remove. 

10.  To  all  of  the  tubes  add  2  units  of  amboceptor  and 
1  c.c.  of  the  suspension  of  sheep's  red  blood  cor- 
puscles. 

11.  Incubate  2  hours. 

12.  Remove  and  then  place  on  ice  20  hours. 

REACTION.  Hemolysis  should  be  complete  in  the  rear  row 
of  tubes  and  in  the  tube  No.  5  in  the  front  row  containing 
normal  serum. 

Complete  inhibition  in  No.  1. 

No.  3,  containing  the  patient's  serum,  will  show  in- 
hibition of  hemolysis  of  various  intensities  if  the  patient 
be   infected   with   syphilis. 

DEDUCTIONS   FROM   THE  WASSERMANN   TEST. 

Note. — The  syphilitic  antibody  present  in  the  pa- 
tient's serum  may  vary  in  amount,  hence  the  comple- 
ment may  be  fixed  to  a  variable  degree.  When  com- 
plement is  fixed,  it  can  no  longer  act  in  conjunction 
with  amboceptor  in  that  process  known  as  hemolysis. 
In  other  words,  hemolysis  in  inhibited  in  varying 
degrees  depending  upon  the  amount  of  syphilitic  anti- 
body present. 

(a)  If  complete  inhibition  of  hemolysis  be  present 
in  the  tube  containing  0.1  c.c.  serum  and  0.1  c.c. 
antigen,  the  result  is  expressed  by  Citron  thus: 
+  +  +  +  . 

78 


(b)  If  not  complete  in  the  tube  containing  0.1  c.c. 
but  complete  in  the  tube  containing  0.2  c.c,  the 
result  is  expressed  thus:      +  +  +  . 

The    results    in     (a)     and     (b)     are    called 
STRONGLY  POSITIVE. 

(c)  If  hemolysis  be  complete  in  tube  containing  0.1 
c.c.  serum  while  that  containing  0.2  c.c.  shows 
complete  inhibition,  the  result  is  expressed  thus- 

+  +. 

(d)  Incomplete  inhibition  in  the  tube  containing  0  2 
c.c.  is  expressed  thus:      +. 

The    results    in     (c)     and    (dj     are    called 
WEAKLY  POSITIVE. 

(e)  When  inhibition  in  the  tube  containing  0.2  c.c. 
is  doubtful,  the  result  is  expressed  thus:     ±. 


2.     Noguchi  Modification. 

It  has  been  found  that  human  serum  contains  a  variable 
amount  of  natural  sheep  amboceptor.  For  this  reason,  Noguchi 
employs  an  anti-human  hemolytic  system  to  replace  the  anti- 
sheep  hemolytic   system  of  the   original   Wassermann. 

Five  factors  enter  into  the  Noguchi  modification  (as  in 
all  others) : —  ^ 

1.     ANTI-HUMAN    HEMOLYTIC  AMBOCEPTOR. 

Rabbits  are  immunized  with  human  R.  B.  C. 
Preparation. 

Rabbits  are  injected  (intraperitoneally)  with  in- 
creasing doses  of  washed  human  R.  B.  C.  allowing 
5  days  to  elapse  between  each  injection. 

1st   injection 5  c.c.  washed  human  R.  B.  C. 

2nd  injection 8  c.c.  washed  human  R.  B.  C. 

3rd  injection 12  c.c.  washed  human  R.  B.  C. 

4th  injection 15  c.c.  washed  human  R.  B.  C. 

5th  injection 20  c.c.  washed  human  R.  B.  C. 

The  serum  is  collected  from  the  immunized  ani- 
mal 9  or  10  days  after  the  last  injection  by  bleeding 
the  rabbit   (from  carotid  artery). 

[The  corpuscles  must  be  washed  at  least  3  times 
with  large  amount  of  saline  solution  (0.9%).] 

79 


Having  collected  the  blood,  allow  same  to  stand 
at  room  temperature  for  several  hours  during  which 
time  coagulation  occurs.  If  the  clot  does  not  con- 
tract within  4  or  5  hours  and  remains  adherent  to  the 
sides  of  the  tube,  insert  a  platinum  needle  (sterile) 
between  the  clot  and  the  walls  of  the  tube  and  detach 
the  clot.  Allow  this  to  remain  4  or  5  hours  again  at 
room  temperature. 

Now  place  in  refrigerator  for  24  hours.  Cen- 
trifuge. 

Decant  supernatent  serum.  For  about  3  days 
after,  some  more  serum  will  exude  and  this  can  be 
also  utilized.  These  daily  sera  may  be  mixed  to- 
gether. 

If  the  serum  be  not  clear,  it  may  be  clarified  by 
centrifugalization  or  by  permitting  the  tube  to  stand 
— when  sedimentation  occurs  and  then  decanting. 

Amboceptor  must  be  titrated.  The  titre  of  the 
serum  is  expressed  by  the  smallest  amount  of  serum 
which  is  found  to  be  necessary  for  complete  dissolu- 
tion of  a  fixed  amount  of  red  blood  corpuscles  and  a 
fixed  amount  of  complement. 

A  good  preparation  will  have  the  value  of  one 
unit  in  something  less  than  0.001  c.c.  of  serum,  that 
is,  0.001  of  serum  or  less,  will  cause  complete  hemo- 
lysis of  1  c.c.  of  a  1%  suspension  of  human  R.  B.  C. 
when  combined  with  0.02  c.c.  of  guinea-pig's  fresh 
serum   (0.1  c.c.  of  209o   dilution). 

2.  PATIENT'S  SERUM  TO  BE  TESTED. 

With  a  Hagedorn  needle  puncture  the  skin  over 
the  last  joint  of  the  middle  finger    (ventral  aspect). 

Collect  the  exuding  drops  in  a  Wright's  blood 
capsule  through  the  curved  end  of  same. 

Seal  the  straight  capillary  end  by  a  flame  and 
shake  the  blood  down  into  this  end  after  the  capsule 
has  cooled. 

Then  seal  the  other  end. 

The  blood  clots  in  the  capsule  and  serum  exudes. 

When  ready  for  the  test  break  the  capsule. 

3.  HUMAN   CORPUSCLE   SUSPENSION. 

Into  a  10  c.c.  graduated  centrifuge  tube  place 
9  c.c,  of  the  following  citrate  solution. 

80 


Sodium  citrate 20  G 

Normal  salt  sol.   (O.dVo) .".1000  c.c. 

Permit  the  blood  of  a  normal  person  to  drop  into 

this  mixture  until  the   volume  in  the  tube   registers 

10  c.c.     Mix  well  and  centrifuge. 

Pour  off  the  supernatent  liquid  and  fill  tube  again 
with  salt  solution. 

Mix  again,  centrifuge,  and  again  decant  super- 
natent fluid  leaving  a  deposit  containing  corpuscles 
freed  from  serum. 

Now  resuspend  the  corpuscles  in  salt  solution 
To  make  a  1%  suspension,  add  100  c.c.  salt  solution 
To  make  a  10%  suspension,  add  10  c.c.  salt  solution! 

We   may  use  these  standard   suspensions   in  the 
proportion  of  1  c.c.  of  the  1%   solution  or  0  1  c  c    of 
the  10%  solution.     The  latter  one  is  preferred. 
4.     GUINEA-PIG'S   SERUM    AS   COMPLEMENT. 

Bleed  the  normal  guinea-pig  at  the  carotid  artery 
allowing  blood  to  flow  into  large  Petri  dish. 

Cover  dish  and  allow  to  stand  at  room  tempera- 
ture for  a  few  hours  when  coagulation  will  have  oc- 
curred and  serum  exuded. 

To  complete  the  separation  of  the  serum,  the  dish 
may  be  placed  in  a  refrigerator. 

After  5  to  10  hours  decant  the  serum  into  a  test 
tube  and  keep  in  a  refrigerator  when  not  in  use. 

Since  complement  deteriorates  in  24  hours,  blood 
may  be  aspirated  directly  from  the  guinea-pig's  heart. 

The  dilution  used  is  40%.  One  c.c.  of  comple- 
ment is  mixed  with  11/2  c.c.  of  physiological  salt 
solution. 

(The  guinea-pig  will  stand  the  loss  of  5  to  10  c.c. 
blood  but  don't  puncture  again  until  after  28  days 
have  elapsed.) 

5.     ANTIGEN.     (Preparation.) 

Extract  a  mashed  paste  of  liver,  heart  or  kidney 
of  man,  ox,  guinea-pig,  rabbit  or  dog  with 

Ten  parts  absolute  alcohol  at  37"  C.  for  several 
days. 

Filter  through  filter  paper  and  collect  the  filtrate. 
Allow  the   filtrate  to   evaporate   to   dryness   with 
the  assistance  of  an  electric  fan. 

81 


Take  up  the  dried  residue  with  ether  and  permit 
the  turbid  solution  to  stand  in  a  covered  dish  in  a 
cool  place  over  night.  In  the  morning,  the  turbidity 
will  have  disappeared. 

Decant  the  clear  etherial  solution  into  a  clean 
beaker  and  concentrate  by  evaporating  most  of  the 
ether. 

Mix  this  concentrated  solution  with  10  volumes 
of  pure  acetone. 

Allow  precipitate  to  settle  and  decant  supernatent 
fluid. 

This  antigen  is  a  slightly  brownish  precipitate 
which  gradually  becomes  sticky  on  exposure  to  air. 

This  acetone-insoluble  portion  of  the  tissue  extract 
containing  antigenic  lipoids  must  be  examined  for 
its  quality  and  strength  and  more  especially  with  re- 
gard to  its  hemolytic  and  anti-complementary  actions. 

By  anti-complementary  action,  we  mean  a  diminu- 
tion or  a  destruction  of  the  activity  of  the  complement. 
To  make  a  stock  solution: 

3/10   G.   of  this  acetone-insoluble  fraction  is 

dissolved  in   1   c.c.   ether  and  mixed  with   9  .c.c. 

methyl  alcohol. 

If  any  precipitate  forms  or  is  left  undissolved, 

remove  by  centrifugation. 

The    stock    solution   contains    3%    of   lipoids 

from  which  an  emulsion  can  be  made  when  ready 

for  it. 
The  emulsion  is  made  by  mixing 

1  c.c.  of   the   stock   solution  with 

9  c.c.  physiological  salt  solution. 

This  produces  a  clear  opalescent  solution  con- 
taining 0.3%  of  the  original  lipoids.    We  only  use 

1/10  c.c.  of  this  emulsion  in  the  test. 

The   antigenic  property  of  the  extract  must 

be   determined,   that  is,   its  power  of  production 

of  complement  fixation  in  the  presence  of  syph- 
ilitic serum. 
1.     Test  for  hemolytic  action  of  antigen. 

Antigen    emulsion 0.4  c.c. 

Salt  solution 0.6  c.c. 

10%   corpuscle  suspension 0.1  c.c. 

Incubate  at  37°  C.  for  2  hours. 

82 


2.  Test  for  anti-complementary  action  of  antigen. 

Antigen    emulsion 0.4  c.c. 

Salt  solution 0.6  c.c, 

40%    complement o.l  c.c. 

Amboceptor 2  units 

Incubate  at  37"  C.  for  1  hour. 

Corpuscle  suspension  10% 0.1  c.c. 

Incubate  at  37''  C.  for  2  hours. 

3.  Test  for  antigenic  property. 

Antigen  emulsion  (1 :  10) 0.2  c.c. 

Salt  solution   0.8 

Syphilitic  serum 0.02 

(1  drop  from  a  capillary  pipette) 

40  %    complement 0.1 

Amboceptor 2  units 

Incubate  at  37°  C.  for  1  hour. 

10%   corpuscle  suspension 0.1  c.c. 

Incubate  at  37°  C.  for  2  hours. 

Noguchi  claims  that  at  least  4  antigen  doses  must 
be  used.  To  obtain  this  he  recommends  the  use  of 
a  0.1  c.c.  of  a  0.3%  suspension  of  acetone-insoluble 
tissue  lipoids.  In  this  quantity  there  will  be  at  least 
5  antigen  doses  (0.1  c.c. ^0.02  c.c. =5). 

TECHNIC   (of  the   Noguchi   modification). 

Arrange  6  test-tubes  in 
pairs  as  shown  in  the  il- 
lustration. 


z 


4 


6 


3 


Into  No.  1  and  No.  2 
place  one  drop  (0.2  c.c.) 
(from  a  capillary  pipette)' 
of  the  patient's  serum  to 
be  tested. 

Into  No.  3  and  No.  4 
(which  are  to  serve  as 
positive  controls)  place  one 
drop  of  the  serum  of  a  per- 
son known  to  be  syphilitic 
or  who  have  given  a  posi- 
tive reaction. 

Into  No.  5  and  No.  6 
place  one  drop  of  the 
serum  of  a  normal  individ- 
ual. These  are  called  neg- 
ative controls. 


83 


To  each  of  the  6  tubes  add  1  c.c.  of  the  suspension 
of  washed  human  corpuscles  and  0.04  c.c.  fresh  guinea- 
pig  serum  as  complement. 

To  tubes  1,  3  and  5,  add  one  drop  of  the  antigen 
solution. 

Shake  all  tubes  vigorously  and  incubate  for  1  hour 
at  a  temperature  of  37°  C. 

Then  add  2  units  of  anti-human  amboceptor  to  each 
of  the  six  tubes  and  shake  well. 

Incubate  all  the  tubes  at  37°  C.  for  1  hour  more. 

Remove  'from  incubator  and  permit  to  stand  at  room, 
temperature  for  the  next  10  or  12  hours  during  which 
time  the  reaction  may  be  watched  as  it  progresses  and 
read. 

Deductions.  The  3  even-numbered  tubes  should  show 
complete  hemolysis.  The  color  should  be  uniformly 
red  but  no  corpuscular  sediment. 

Tube  No.  5  should  show  complete  hemolysis  be- 
fore the  final  reading  is  made. 

Tube  No.   3   will  be   clear. 

Tube  No.  1:  if  it  resembles  No.  3,  reaction  is 
positive;  if  it  resembles  Nos.  2,  4  or  6,  reaction  is 
negative. 


3.     Method  of  Cyrus  W.  Field. 

He  employs  cholesterinized  antigen.  The  velocity  of  the 
test  seems  to  be  increased  thereby.  Each  c.c.  of  the  diluted 
antigen  contains  0.1  mg.  of  the  combined  lipoids  and  choles- 
terin.  It  is  easily  prepared  and  is  rarely,  if  ever,  anti-com- 
plementary or  hemolytic  as  are  the  Wassermann  and  Noguchi 
antigens.  The  essential  point  in  this  method  is  the  standard- 
ization of  antigen,  which  means  that  irrespective  where  the 
test  is  made,  whether  in  New  York,  San  Francisco  or  New 
Orleans,  the  results  will  always  be  the  same. 

Antigen.  Alcoholic  extract  of  a  large  number  of  guinea-pig's 
hearts  with  one-half  saturation  with  cholesterin.  20  c.c. 
of  this  cholesterinized  extract  is  evaporated  and  dessicated 
and  the  residue  weighed. 

The  extract  is  then  used  in  such  dilution  that  1  c.c. 
thereof  represents  1  mgm.  of  the  cholesterin  lipoids. 

84 


CORRECTION. 

Transpose  line  9  which  reads  "Add  the  antigen,  comple- 
ment (v/hich  is  usually  0.5"  immediately  before  line  14.^  It 
will   then  read:  — 

Add  the  antigen,  complement  (which  is  usually  u.5 
c.c.  of  a  1:8  dilution)  to  the  serum  and  incubate  for  40 
to  50  minutes  at  37°  C. 


SB«^w:_ 


Anti-sheep   hemolytic  amboceptor. 

Complement  in  the  dilution  of  3:8.     At  least  2  units  of  am- 
boceptor and  21/^  units  of  complement  should  be  used. 

Technic: 

Racks  holding  8  tubes  are  set  up.  Label  consecutively 
from  1  to  8. 

Into  each  of  7  tubes  place  0.1  c.c.  of  the  patient's 
serum. 

Add   the   antigen,    complement    (which  is   usually   0.5 

Into    the    8th    tube    place    twice    that    amount    (0.2). 

(Tubes  No.  1  and  No.  8  are  used  as  controls.) 

To   the  other   6   tubes   add   antigen   in   the   following 

amounts:      (expressed  in  c.c.)  1,  0.8,  0.6,  0.4,  0.2  and  0.09. 

c.c.  of  a  1:8  dilution)   to  the  serum  and  incubate  for  40 

to  50  minutes  at  37'  C. 

Mix  the  amboceptor  and  the  suspension  of  R.  B.  C. 
in  their  proper  proportions  and  add  sufficient  salt  solu- 
tion so  that  each  c.c.  of  the  mixture  represents  at  least 
2  units  of  amboceptor  and  0.5  c.c.  erythrocytes.  The 
mixture  is  incubated  at  least  30  minutes  before  being 
mixed  with  the  serum-antigen-complement  mixture. 

The  results  are  read  off  as  soon  as  the  2  control 
tubes  show  complete  hemolysis  and  labeled  according  to 
the  following  scheme: 

0.  Represents   complete   hemolysis,   while 

1.  Slight  inhibition  of  hemolysis,  w^hile 

2.  Marked  inhibition  of  hemolysis,  while 

3.  Complete  inhibition  of  hemolysis. 


SERO-DIAGNOSIS  OF  PREGNANCY. 

Abderhalden's  Test. 

The  DIALYZATION  METHOD  is  preferred  to  the  Optic  Method. 

The  basis  of  the  test  consists  in  the  conversion  of 
colloidal  non-dialyzable  placental  proteid  into  dialyzable 
products  through  the  activity  of  certain  ferments. 

These  products  may  then  be  detected  by  simple  color 
reactions  in  the  dialysate. 

85 


THINGS   NECESSARY   FOR  THE  TEST. 

1.  Fresh  coagulated  placental  proteid  (albumin). 

2.  Blood.  Ten  c.c.  venous  blood  from  suspected  female 
is  centrifuged.  Serum  is  drawn  off  into  a  clean  sterile 
tube. 

Note.^ — Since  the  amino  acids  which  form  during 
digestion  may  give  a  positive  reaction  with  triketohy- 
drinden  hydrate,  all  blood  specimens  should  be  taken 
before   breakfast. 

3.  DIalyzing  tubes.  The  dialyzing  thimbles  must  be  per- 
meable for  peptones  but  not  for  albumin. 

TECHNIC. 

1.  Into  each  of  3  thimbles  place  1  G.  of  coagulated  pla- 
cental proteid  (albumin)  which  has  been  washed  in 
distilled  water,  dried  between  filter  paper  and  ground 
up  in  a  mortar. 

2.  To  thimble  No.  1,  add  2  or  3  c.c.  of  hemoglobin-free 
serum  to  be  tested.     Overlay  this  mixture  with  toluol. 

3.  Place  thimble,  et  al.,  in  a  sterile  dialyzing  tube  con- 
taining 20  c.c.  distilled  water  which  should  stand 
slightly  higher  than  the  fluid  in  the  thimble. 

4.  Overlay  the  external  fluids  with  toluol  and  plug  the 
dialyzing  vessel  with  cotton  to  hold  in  place  the 
thread  which  suspends  the  shell. 

5.  Incubate  at  37°  C.  for  18  hours.  Then  test  the  dialy- 
sate  for  peptone. 

6.  Thimbles  number  2  and  3  are  controls. 

In  Thimble  No.  2.  Place  1  G  placental  albumin  and 
2  c.c.  of  a  serum  of  a  known  positive  control. 
Overlay  with  toluol  and  proceed  as  above. 

In  Thimble  No.  3.  Place  1  G  placental  peptone  and 
2  c.c.  of  a  known  negative  serum  or  with  the  in- 
activated (heated  to  60°  C.)  serum  used  in  the  test. 

Serum  control.    A  thimble  containing  only  2  c.c.  serum. 

TESTS  FOR  THE  "CLEAVAGE  PRODUCTS"  OF  ALBUMIN. 

(A)  Biuret  test. 

(B)  Ninhydrin   or   Triketohydrinden    Hydrate    reaction. 
This  is  preferred  to  the  Biuret  test. 

86 


NINHYDRIN    REACTION. 

1.  Remove  10  c.c.  of  the 
dialysate  by  means  of  a 
pipette  dipping  below  the 
toluol  and  place  this  in  a 
large  test  tube. 

2.  Add  0.2  c.c.  of  a  watery 
solution  of  ninhydrin 
(1%). 

3.  Heat  rapidly  to  boiling 
point  and  keep  boiling  1 
minute. 

Positive  reaction.  A  deep 
blue  color  appears  imme- 
diately or  after  standing  a 
short  time. 

Negative  reaction.  Either  no 
coloration  at  all  or  perhaps 
a  slight  yellow. 

Time  of  appearance.  Reac- 
tion may  be  obtained  in 
middle  of  the  second  month. 

Reaction  disappears  in  from 
10  to  15  days  after  delivery. 


BIURET  TEST. 

1.  Remove  10  c.c.  of  the 
dialysate  as  in  other 
method. 


2.  Add  5  c.c.  of  33%  sodium 
hydroxide  solution  and 
mix. 

3.  Titrate  from  a  biuret  with 
0.25%  copper  solution 
drop  by  drop  in  such  a 
manner  as  to  form  a 
"contact  ring." 

Positive     reaction.       Peptone 

yields  a  violet  red  to  a  pure 
red  contact  ring  sharply 
differentiated  from  the 
lower  colorless  and  upper 
blue  solutions. 


Negative     reaction. 

bluish  ring. 


Distinct 


87 


CHAPTER  IV. 

FORENSIC  MEDICINE. 
Tests  for  Blood. 

INTRODUCTION. 

In  medico-legal  cases,   no  tests   for  blood   should  be 
performed   until   the   following   points   have   been   noted: 

1.  The  exact  time  and  exact  part  of  the  clothing  or 
other  object  from  which  the  specimen  was  taken. 

2.  If  the  blood  is  to  be  scraped  from  an  instrument,  de- 
scribe fully. 

3.  Note  shape  and  size  and  direction  of  all  stains.  (The 
small  part  of  the  spatter  points  to  the  opposite  direc- 
tion of  the  hemorrhage. 

4.  Specimens  sent  to  you  must  have  been  properly 
sealed;  the  sender's  name  recorded;  date  and  time 
of  delivery  noted,  and  seal  must  be  unbroken. 

5.  Examine  only  a  small  portion  of  the  specimen.  Keep 
the  remainder  for  corroborative  evidence. 

SPECIAL   REMARKS. 

1.  Before  giving  an  opinion,  it  is  well  to  remember  that 
blood  cannot  always  be  differentiated  with  absolute 
certainty  from  blood  from  other  sources. 

2.  Blood  appearing  on  one's  person  may  be  there  acci- 
dentally by  reason  of  one's  occupation,  e.  g.,  butchers. 
Or,   in  women,   menstrual   blood  must  be   considered. 

3.  Time  not  only  alters  the  appearance  of  blood,  but 
also  influences  the  tests  for  blood. 

4.  Blood  stains  upon  a  knife  or  other  metal  must  be  dis- 
tinguished from  rust  or  lemon  stains.  All  weapons 
should  be  examined  immediately, 

5.  Blood  stiffens  all  fabrics.  Under  a  hand  microscope, 
blood  stains  on  linen  give  a  dark  crimson  reflection, 
are   glossy,   smooth  or  reddish  brown. 

6.  The  action  of  various  substances  such  as  mortar, 
brick,  lime,  strong  acids  or  alkalies,  leather,  chemicals 
in  wall  paper,  starched  clothing,  etc.,  may  so  change 
the  blood  or  impair  its  reactivity  to  certain  tests  so 
that  no  definite  conclusions  can  be  drawn. 

88 


1.     Finding  Red  Cells  in  Dissolved  Stains. 

(Is   the   Surest    Proof   of    Blood.) 

COMPARATIVELY   RECENT  STAINS, 

Are  soluble  In  cold  water. 

The  R.  B.  C.  are,  however,  somewhat  deformed  but 
present  the  morphological  characteristics  described  on 
p.  34. 

Mammalian  R.  B.  C.  with  few  exceptions  are  circular 
and  non-nucleated. 

Oviparse  are  ovoid  in  shape  and  show  a  central  ag- 
gregation of  granules  resembling  a  nucleus. 

Mammalian  corpuscles  are  the  smallest  of  all  ex- 
cepting the  musk-deer   (1/12,000  of  an  inch). 

The  corpuscles  of  reptiles  are  the  largest. 

The  central  granules  above  described  can  be  made 
more  distinct  by  adding  acetic  acid. 

The  corpuscles  are  small  in  elephants,  pigeons  and 
toads. 

When  a  stain  is  dissolved  in  water,  the  color  of  the 
solution  is  found  to  vary  with  the  age  of  the  stain. 

A  very  recent  stain  produces  a  bright  red  solution 
owing  to  the  passing  out  of  the  Hb.  from  the  R.  B.  C. 
into  the  water   (hemolysis). 

OLDER   STAINS. 

Hemoglobin  is  less  soluble  and  methemoglobin  is  the 
result. 

EXCEEDINGLY  OLD  STAINS. 

Insoluble  in  water;  soluble  in  dilute  citric  acid  and 
in  ammonia  water. 

A  clot  can  be  disintegrated  by  dissolving  its  albumin 
with  a  33  7o  solution  of  KOH  or  a  50  Sc  glycerine  solution. 
The  best  examining  fluid  is  Marx's  fluid.  It  stains  the 
R.  B.  C.  red.     It  consists  of: 

Quinine  hydrochlorate  (1:1,000  sol.) 10  c.c. 

Potassium  hydrate   (339c  sol.) -. 10  c.c. 

Eosin,  q.  s,  to  tint. 


2.    Julius  von  Kossa's  Test. 

1.  Take  10  c.c.  of  the  watery  solution  to  be  tested. 

2.  Add  10  c.c.  of  907c  alcohol  and  5  c.c.  chloroform. 

3.     Mix  gently  but  DO  NOT  SHAKE. 

89 


Positive  reaction.     The  hemoglobin  is  dissolved  and  appears 
on  top  of  the  layer  of  chloroform  as  tiny  red  droplets. 

For   urine.     Use   10   c.c.   urine,   10   c.c.   distilled  water,   5   c.c. 
alcohol,  5  c.c.  chloroform  and  mix  gently. 


3.     Van  Deen's  Guaiac  Test. 

1.  To  any  volume  of  the  watery  solution  to  be  tested  add  an 
equal  volume  of  freshly  prepared  guaiacum  resin  in  al- 
cohol. 

2.  By  floating  either  (a)  peroxide  of  hydrogen,  (b)  ozonized 
oil  of  turpentine,  or  (c)  oil  of  eucalyptus  a  blue  sapphire 
color  is  immediately  formed  at  the  point  of  contact  and 
on  shaking  the  color  will  spread  throughout  the  mixture. 

3.  If  the  stain  be  very  old,  apply  the  chemicals  direct  on 
the  fabric  and  immediately  place  a  piece  of  filter  paper 
on  the  spot  and  the  latter  will  turn  blue. 

Note. — The  blue  color  must  occur  after  the  peroxide 
is  added.     It  is  a  good  confirmatory  test. 

Test  may  not  be  obtained  after  stain  is  2i/^  years  old. 

It  is  more  reliable  in  its  negative  phase  than  when 
positive  because  many  other  substances  give  a  positive 
reaction.     They   are: 


Potassium  permanganate. 
Peroxide  of  lead. 
Peroxide  of  manganese. 
The  halogen  group. 
Nitric  and  chromic  acids. 
Ferric  chloride, 
Copper  salts. 


Potassium  ferro-  and  ferri- 
cyanide. 

Gum  acacia. 

Gluten. 

Unboiled  milk. 

Raw  potato  pulp. 

Pus. 

Any  living  cell  or  its  intra- 
cellular enzymes. 


4.     Schaer's  Test. 

Teclinic.  Similar  to  that  of  the  guaiac  test  excepting  that  a 
1  to  4%  solution  of  aloin  in  alcohol  is  used  instead  of 
guaiac. 

Positive   reaction. 

1.  When  the  tincture  of  aloin  is  added  to  the  suspected 
solution  a  red  color  appears,  quickly  assuming  a 
cherry-red  appearance  when  ozonized  oil  of  turpentine 
is  added. 

90 


The  pink  color  should  develop  within  a  short  time. 
There  are  substances  which  produce  this  coloration 
in  a  few  hours. 

Note. — The  tincture  should  be  freshly  prepared 
because  such  color  changes  occur  spontaneously  of 
itself  on  standing. 


5.     Phenolphthalein  Test. 

1.  To  1  part  of  the  watery  solution  of  blood  to  be  tested  add 

2.  Two  parts  of  the  following  reagent  prepared  thus: 

(a)  Mix  1  c.c.  of  N/10  NaOH  with  a  few  c.c.  distilled 
water,  with  a  slight  excess  of  phenolphthalein. 

(b)  Shake  thoroughly  and  filter. 

(c)  To  the  filtrate  add: 

Sodium    hydrate 20      c.c. 

Peroxide  hydrogen  (3'/o) 0.1  c.c. 

And  make  up  to IQO      c.c. 

Allow  to  stand  a  few  minutes. 

Note. — Fresh    solutions   are    devoid   of   any   pink 
coloration  but  will  be   so  in  time. 

Positive  reaction.  A  pink  to  a  red  color  depending  upon  the 
amount  of  blood  present.  The  test  is  so  delicate  that  it 
will  detect  blocd  even  in  the  proportion  of  one  part  blood 
to  eight  million  of  water. 

Testing  for  blocd  in  the  secretions  and  excretions. 

1.  Extracts  of  various  animal  tissues  or  various  secre- 
tions of  the  body  interfere  with  the  test  so  that  blood 
cannot  be  recognized  in  such  great  dilutions  as  when 
watery  solutions  are  employed. 

2.  Boiling  these  solutions  prior  to  the  test  removes  most 
of  the  objections.     Or, 

3.  If  the  secretions  be  treated  with  a  thick  cream  of 
aluminium  hydrate  suspension,  the  precipitate  will 
carry  down  the  blood  pigment  and  thus  concentrate 
it. 

A  small  amount  of  this  precipitate  (whether  de- 
rived from  urine,  feces  suspension,  exudates,  etc.), 
will  show  a  decided  color  when  added  to  2  c.c.  of  the 
reagent. 

91 


6.     Teichmann's  Hemin  Crystals. 

1.  Place  some  dried  blood  on  a  slide  and  add  a  drop  or  two 
of  glacial  acetic  acid.     Cover  with  cover  slip. 

2.  Two  drops  of  common  salt  solution  (2  grains  to  8  ounces 
of  water)   are  added  in  case  the  blood  is  very  old. 

3.  Heat  the  slide  gently  so  that  the  fluid  steams  but  does  not 
boil.  As  the  acid  evaporates,  allow  more  to  run  under 
the  cover  slip. 

4.  After  the  slide  cools  mount  in  glycerine. 

Positive  reaction.  Dark  brown  rhombic  plates  and  prisms 
appear.  Star-shaped  clusters  with  rounded  angles  are  also 
quite  common.  The  crystals  cross  each  other  so  as  to 
resemble  the  letter  "X." 

The  reaction  may  thus  be  expressed: 

Hemoglobin -(-acetic  acid-j-NaCl=globin-|-HCl+hematin; 

Hematin-|-HCl=Hemin  crystals    (hydrochlorate  of  hema- 

tin). 

Note. — If  blood  be  mixed  with  iron  rust,  the  hematin 
test  will  be  negative. 


7.     Spectroscopic  Absorption  Bands. 

Introduction.  The  various  solutions  of  hemoglobin  and  its 
derivatives  produce  characteristic  absorption  bands  which 
always  occupy  definite  and  constant  positions  with  rela- 
tion to  the  Fraunhofer's  lines. 

These  lines  are  vertically  placed  and  appear  as  dark 
slits.     They  are  8  in  number  and  lettered  from  A  to  H. 

Recent  stains. 

If  on  fabric,  cut  it  in  small  strips  and  place  into  glass- 
stoppered  vials  (capacity  of  i/4-ounce,  but  only  %  full 
with  distilled  water). 

When  the  solution  becomes  red  or  reddish  brown 
remove  some  of  it  by  means  of  a  capillary  pipette  and 
insert  it  into  the  cell  chamber  of  Zeiss's  Microspectro- 
scope  and  examine  for  absorption  bands. 

It  is  to  be  especially  noted  that  bands  are  only  visible 
when  the  solutions  are  of  a  certain  strength  and  certain 
depth   (depth  of  1  cm.  and  strength  of  0.85  to  0.65%). 

92 


Oxyhemoglobin. 

In  the  above  dilution  and  depth  2  bands  are  seen 
between  the  D  and  E  positions. 

The  alpha  band  nearest  D  being  narrower  but  darker 
than  the  beta  band  nearest  E. 

In  weaker  dilutions,  the  beta  band  disappears  first. 

With  greater  concentration,  the  two  bands  become 
broader  and  the  space  between  them  narrower  and  the 
blue  and  violet  ends  of  the  spectrum  disappear. 

By  adding  a  particle  of  ferrous  sulphate,  a  particle 
of  Rochelle  salt  and  a  little  ammonia,  the  two  bands  are 
reduced  to  one  band.  This  is  called  reduced  hemoglobin 
or  Stoke's  band  (the  ingredients  given  above  forming 
Stoke's  reagent. 

Hemoglobin,  also  called  reduced  hemoglobin,  is  more 

soluble  than  oxyhemoglobin. 

Its  solutions  are  more  violet  or  purplish  than  those 
of  oxyhemoglobin  of  the  same  strength. 

Hemoglobin  solutions  absorb  the  blue  and  violet 
rays  to  a  less  extent  than  those  of  oxyhemoglobin  but 
they  strongly  absorb  the  rays  lying  between  the  C  and  D 
lines. 

As  before  stated,  with  proper  dilution,  its  spectrum 
is  that  of  one  broad  band  not  clearly  defined  between  D 
and  E,  lying  towards  the  red  end  of  the  spectrum  a  little 
over  the  D  line. 

Old  stains.  Oxyhemoglobin  having  been  converted  into  hema- 
tin  which  is  insoluble  in  water,  it  becomes  necessary  to 
add  a  few  drops  of  acetic  acid  and  the  bottle  must  be  per- 
mitted to  stand  in  a  warm  place  for  several  hours. 

Examine  some  of  this  solution  for  acid  hematin 
bands.     The  bands  can  be  reduced  by  Stoke's  reagent. 

ACID   HEMATIN   shows  4  bands: 

1.  Between  C  and  D. 

2.  1    Another  broad  band  not  clearly  defined   between  D 

3.  J    and  F,  which,  under  certain  conditions  divides  into  2 

narrower  bands. 

4.  A  fourth  band  between  D  and  E,  which  is  nearer  D 
and  very  weak. 

ALKALINE   HEMATIN: 

One  band  between  C  and  D  which  reaches  out  to  some 
extent  between  D  and  E. 

93 


If  this  alkaline  solution  be  reduced  with,  ammonium 
sulphide  we  obtain  the  spectrum  of  hemochromogen. 

HEMOCHROMOGEN.     Shows  2  bands: 

1.  Is  very  sharp  and  dark  betv\^een  D  and  E, 

2.  Paler  and  broader  band  covering  the  E  line. 

HEMATOPCRPHYRIN. 

Is  isomeric  with  bilirubin  and  is  formed  when  hema- 
tin  is  treated  with  concentrated  sulphuric  acid  in  the  pres- 
ence of  air.  It  loses  its  iron  constituent.  It  is  insoluble 
in  water. 

In  acid  solution.     Two  bands. 

1.  A  faint  and  narrow  band  between  C  and  D  but  nearer 
D. 

2.  Another    darker,    sharper    and    broader    band    in    the 
middle  between  D  and  E. 

In  dilute  alkaline  solution.     Four  bands. 

1.  One  band  between  C  and  D. 

2.  A  broad  band  covering  D  but  its  broadest  portion  be- 
tween D  and  E. 

3.  Between  D  and  E,  nearly  at  E. 

4.  A  fourth  band,  broad  and  dark  between  E  and  F. 

Importance.  Medico-legally  very  important  because 
certain  old  stains  can  be  identified  only  by  its  spectrum. 

METHEMOGLOBIN. 

In  watery  or  slightly  acid  solution. 

Its  spectrum  resembles  that  of  acid  hematin  but  with 
this  difference:  it  easily  is  converted  into  hemoglobin 
by  reduction  with  alkali.  On  the  other  hand,  when  acid 
hematin  is  reduced  it  is  converted  into  hemochromogen. 

In  alkaline  solution. 

Its  spectrum  resembles  that  of  oxyhemoglobin  but 
with  this  difference:  that  the  band  nearest  E  is  stronger 
than  that  at  D.  According  to  Hammersten  a  third  band 
occurs  between  C  and  D. 

Significance.  Occurs  in  cases  of  poisoning  with:  potas- 
sium permanganate,  potassium  ferricyanide,  chlorates, 
nitrites,  nitrobenzol,  acetanilide,  antipyrin,  turpen- 
tine, sulphonal,  arsenic  and  in  cases  of  cyanosis  with 
diarrhea.  Hemorrhagic  transudates  and  cystic  fluids 
due  to  spontaneous  decomposition  of  blood. 

94 


CARBON  MONOXIDE  HEMOGLOBIN. 

Two  bands  between  the  D  and  E  lines  but  they  are 
situated  more  to  the  left  (violet  end)  of  the  spectrum. 
It  cannot  be  reduced. 

It  is  found  after  coal  gas  or  illuminating  gas  inhala- 
tion and  may  even  be  demonstrated  for  a  short  time  after 
death. 

In  severe  but  not  fatal  cases  it  may  persist  for  sev- 
eral days. 


8.     The  Precipitin  Reaction. 

NOTE. — This  test  is  used  medico-legally  for  the  detection 
of  blood  and  blood  serum,  but  in  reality  it  is  a  specific  test 
for  blood  proteid  and  not  for  blood.  Other  tests  must  prove 
the  presence  of  blood. 

Soluble  proteid  may  give  this  test  at  a  period  as  late  as 
50  years.     It  is  a  very  delicate  test. 

BASIS.  The  serum  of  an  animal  injected  with  blood  or  blood 
serum  of  another  animal,  shows  the  property,  when  added 
to  an  homologous  serum,  of  precipitating  the  albumin  of 
this  serum  in  the  form  of  a  light  flocculent  precipitate. 
Of  course,  human   serum   is  used  in  medico-legal  cases. 

TECHNIC. 

1.  Add  a  sufficient  amount  of  NaCl  to  the  dried  blood  to 
get  it  in  solution.  If  the  stain  is  upon  clothing,  cut 
the  stain  out,  tease  it  and  allow  it  to  stand  in  salt  solu- 
tion one  hour,     (Old  stain  24  hours). 

2.  Filter  these  solutions  twice. 

Once  through  hardened  filter  paper. 
Then  through  a  small  Berkefeld  filter. 

3.  Add  a  sufficient  amount  of  salt  solution  to  make  ap- 
proximately a  1:1,000  solution  of  the  stain.  This  fil- 
trate must  be  clear  and  neutralized  by  adding  some 
tartaric  acid  or  sodium  carbonate  solutions. 

4.  Take  10  test  tubes  of  equal  size  and  thickness.  Label 
them  from  1  up  to  10.     Fill  as  follows: 

Tube  No.     1.     1  c.c.  of  the  above  solution  of  the  stain. 

Tube  No,     2.     1  c.c.  of  the  above  solution  of  the  stain. 

Tube  No.  3.  1  c.c.  of  a  1:1,000  dilution  of  a  known 
fresh  human  blood  in  normal  salt 
solution. 

95 


Tube  No.     4.     1  c.c.   of  a  1:1,000   dried   human   biood 

in  0.9%  salt  solution. 
Tube  No.     5.     1  c.c,  sterile  salt  solution. 
Tube  No.     6.^ 

Tube  No.     7.  I  1  c.c.  of  1:1,000  dilution  of  either  fresh 
Tube  No      R   ^      ^^  dried  blood  of  such  domestic  ani- 
■  I       mals  as   chicken,   dog,   horse,   sheep. 
Tube  No.     9.  J 

Tube  No.  10.  1  c.c.  of  physiological  salt  extract  of 
the  matter  upon  which  the  stain  was 
found. 

To  every  tube  except  No.  2,  allow  0.1  c.c.  anti- 
serum (see  below)  to  trickle  down  from  a  graduated 
pipette  along  the  side  of  the  tubes. 

To  tube  No.  2,  add  0.1  c.c.  of  normal  clear  rabbit 
serum. 

Positive  reaction.  Within  2  minutes,  tubes  1,  3  and  4  which 
contain  human  blood  become  turbid.  The  others  do  not 
contain  blood,  hence  are  clear.     (Contact-ring  turbidity.) 

Preparation  of  Anti-Serum  for  the   Precipitin   Reaction. 

This  is  the  serum  of  the  animal  immunized  against 
the  proteids  of  a  particular  species  of  animal. 

1.  Inject  a  rabbit  intraperitoneally  with  5  to  10  c.c.  of 
whole  blood  or  serum. 

2.  Repeat  said  injections  at  intervals  of  3  to  5  days 
until  6  or  8  injections  have  been  made. 

3.  Allow  one  week  to   elapse  after  the  last  injection. 

4.  Obtain  a  few  drops  of  blood  by  puncturing  rabbit's 
ear  and  allow  same  to  clot  in  a  small  test-tube  and 
the  serum  which  exudes  is  then  tested  for  its  potency. 

(a)  First  make  a  1:1,000  dilution  of  homologous 
blood  in  physiological  salt  (0.9%  NaCl).  Only 
1  c.c.  is  necessary.  Place  in  test  tube.  If  the 
dilution  has  been  properly  made,  a  foamy  layer 
forms  on  shaking  and  if  1  c.c.  of  this  dilution  is 
taken  and  to  it  1  drop  of  a  25%  nitric  acid 
solution   added   a   slight   opalescence   will   occur. 

(b)  Add  the  anti-serum  to  the  above  dilution.  If  a 
turbidity  appears  within  1  to  2  minutes  the  serum 
is  sufficiently  potent  for  the  test. 

5.  Bleed  the  animal.  (Either  partially  or  total  exsan- 
guination.) 

96 


(a)  Collect  blood  in  wide-mouthed  test  tubes  and 
plug  with  cotton.  Allow  to  coagulate  like  agar 
slants. 

(b)  Remove  the  exuded  serum  (which  must  be  clear), 
place  in  test  tubes,  plug  with  cotton,  seal  with 
paraffin,  store  in  refrigerator.  This  is  the  anti- 
serum. 

DIFFERENTIATION   OF   BLOOD   FROM    IRON    RUST. 

Take  some  of  the  rust  on  the  knife  and  place  in  a 
porcelain  capsule  containing  HCl  and  heat  gently. 

If  iron  be  present,  the  solution  becomes  yellow. 

To  potassium  ferrocyanide  add  1  drop  of  the  yellow 
solution  and  the  color  turns  blue. 

To  potassium  sulphocyanide,  add  a  drop  of  this  yel- 
low solution  and  a  deep  red  color  is  the  result. 

DIFFERENTIATION    OF   BLOOD   FROM    RED   PAINT. 

The  pigments  in  red  paint  are  usually  iron  oxide 
and  lead  oxide. 

Dried  paint  is  insoluble  in  water  but  soluble  in  strong 
alkali  solution  or  oil  of  turpentine. 

Take  some  of  this  solution  and  allow  to  evaporate 
upon  a  watch  glass. 

Test  for  iron  as  previously  described. 

Lead  is  recognized  by  its  vermilion  color. 

CHEMICAL   TESTS   for   lead   are: 

1.  The  addition  of  potassium  bichromate  to  any  solu- 
tion containing  lead  causes  the  precipitation  of  a 
yellow  amorphous  deposit,  soluble  in  potassium 
hydroxide  and  strong  HCl,  but  insoluble  in  acetic 
acid. 

2.  Hydrogen  sulphide  passed  through  lead  solutions 
results  in  the  precipitation  of  black  lead  sulphide. 


97 


CHAPTER  V. 

OPSONINS. 

DEFINITION. 

Opsonins  are  certain  substances  probably  belonging  to 
the  class  of  globulins,  present  in  the  blood  serum  which 
render  the  various  forms  of  bacteria  which  invade  the 
body  subject  to  phagocytosis. 

Phagocytosis  signifies  the  power  leucocytes  have 
of  incorporating  in  their  bodies  and  destroying  and  di- 
gesting pathogenic  bacteria.  The  leucocytes,  therefore, 
play  an  important  part  in  immunity. 

Opsonins  may  be  increased  artificially  by  injecting 
certain   bacterial   vaccines. 

Vaccines  are  suspensions  in  physiological  salt  solu- 
tion of  killed  pathogenic  bacteria.  Vaccines  produce  an 
active  immunity;  that  is  to  say,  the  patient  himself  is 
stimulated  to  produce  his  own  antibodies. 

Sera  differ  from  vaccines  in  that  serum  already 
contains  the  antibodies  formed  in  the  body  cells  of  the 
horse  or  other  animal  and  are  simply  supplied  to  the 
patient.  Thus,  passive  immunity  is  established.  Sera 
begin  to  act  shortly  after  injection  w^hile  it  takes  a  few 
days  before  vaccines  begin  to  act.  But,  the  immunity 
established  by  the  use  of  vaccines  lasts  longer  than  in 
the  other  case. 

The  opsonins  differ  according  to  the  various  forms  of 
bacteria  present  in  the  body.  Thus,  the  varying  degree 
of  susceptibility  of  various  persons  to  disease  may  be 
explained.  Clinically,  we  find  a  decrease  in  the  opsonins 
in  certain  bacterial  infections. 

Whenever  a  patient  shows  a  decrease  in  the  phago- 
cytic power  to  any  organism  invading  his  body  and  we 
know  these  infecting  germs,  we  can  increase  his  phago- 
cytic power  by  injecting  him  with  dead  cultures  of  these 
specific  germs.     (Vaccines.) 

Autogenous  vaccines  are  preferable  to  stock  vaccines. 
By  autogenous  vaccines  we  mean  vaccines  made  from  the 
patient's  own  discharges.  For  therapeutic  use  they  are 
better  than  stock  vaccines.  It  is  sure  to  contain  all  the 
germs  responsible  for  the  infection. 

98 


Opsonic  Index.  Expresses  a  comparison  between  the 
phagocytic  power  of  the  patient  to  that  of  a  normal  in- 
dividual. The  number  of  bacteria  incorporated  by  the 
W.  B.  C.  of  such  normal  person  is  regarded  as  one. 

Determination  of  Opsonic  Index.  Four  things  neces- 
sary: 

1.  Patient's  serum. 

2.  Normal  control  serum. 

3.  Washed  leucocytes. 

4.  Bacterial  emulsions. 
Technic. 

1.  Draw  one  volume  of  washed  corpuscles  into  a 
capillary  tube. 

2.  To  it  add  a  similar  volume  of  patient's  serum. 

3.  To  this,  add  a  similar  volume  of  the  specific  bac- 
terial emulsion. 

4.  Blow  these  3  volumes  into  a  dish  and  redraw  up 
into  the  tube.      (This   insures  proper  mixing.) 

5.  Make  another  mixture  like  the  above,  excepting 
that  the  control  serum  is  substituted  for  the  pa- 
tient's serum. 

6.  Incubate  both  for  15  minutes  at  37°  C. 

7.  Blow  1  drop  on  a  glass  slide,  make  a  smear,  fix 
and  then  stain  with  any  of  the  polychrome  dyes 
or  with  special  bacterial  stains. 

8.  Count  about  100  polymorphonuclear  leucocytes 
and  note  the  number  of  germs  incorporated  within 
their  protoplasm.  By  dividing  this  number  by 
100,  we  obtain  the  grand  average  for  one  leu- 
cocyte. This  number  represents  the  phagocytic 
index.  To  obtain  the  opsonic  index,  divide  the 
patient's  value  just  obtained  by  that  of  the  con- 
trol in  paragraph  5  above. 

Vaccines  also  used  for  Diagnostic  Purposes. 

1.  Tuberculin  test ^ 

2.  Moro's  test i   „ 

3.  Von  Pirquet c  '^^^  tuberculosis. 

4.  Calmette  reaction J 

Luetin  reaction For  syphilis. 

99 


K 


HEMATEMESIS— GASTRORRHAGIA. 

DEFINITION. 

A  symptom  denoting  the  appearance  of  blood  in  the 
ejected  gastric  contents. 

ETIOLOGY. 

1.     GASTRIC  CAUSES. 

(a)  Ulcer  of  stomach       > 

/■u^     TT1  ^  ^      I  Usually  chronic. 

(b)  Ulcer  of  duodenum    V 

.   ,      „  ^     .  ,       Multiple  attacks. 

(c)  Cancer  of  stomach  ) 

(d)  Corrosive  poisons 

(e)  Trauma  to  stomach 


r  Usually  acute  attacks. 


2.  HEPATIC   CAUSES. 

(a)  Cirrhosis  of  liver,  especially  atrophic. 

(b)  Passive  congestion  of  liver. 

(c)  Thrombosis    of    portal    vein    or    compression    of 
portal  vein  by  a  tumor. 

3.  SPLENIC   CAUSES. 

(a)  Enlargement,     especially     spleno-medullary     leu- 
kemia. 

(b)  Splenic  anemia. 

4.  TOXIC    CAUSES. 

(a)     Yellow  fever  ("black  vomit.") 

5.  HEMORRHAGIC   DIATHESIS. 

(a)  Hemophilia. 

(b)  Scurvy. 

(c)  Purpura. 

SYMPTOMS  AND    DIAGNOSIS. 

1.  See   under   secondary    (hemorrhagic)    anemia,   p.    6. 

2.  For    differentiation    between    hematemesis    and    hem- 
optysis,  see    p.    104. 

3.  Tests  for  occult   blood   in   gastric   contents. 

100 


SPECIAL   REMARKS:  — 
Atrophic  cirrhosis  of  the   liver. 

Hematemesis  occurs  here  as  one  of  the  so-called 
"obstructive  symptoms." 

In  fact,  hemorrhage  may  occur  anywhere  in  the  hody. 

The  association  of  a  small  liver  with  ascites,  gastro- 
intestinal catarrh,  hematemesis  and  hemorrhoids  is  very 
suspicious  of  atrophic  cirrhosis. 

Following  hematemesis  melaena  may  occur. 

It  is  to  be  specially  noted  that  hemorrhages  from  the 
bowel  may  occur  for  several  years  and  yet  there  be  no 
vomiting  of  blood. 

An  associated  enlarged  spleen  further  accounts  for 
the  hematemesis. 

Hepatic   congestion. 

A  congested  liver  is  often  depleted  by  an  attack  of 
hematemesis. 

In  fact,  hepatic  congestion  most  often  results  from 
chronic  valvular  disease  and  pulmonary  affections.  Hence 
such  losses  of  blood  are  often  attended  by  beneficial  re- 
sults. It  relieves  the  embarrassment  of  the  heart.  The 
improvement  is,  however,  only  temporary. 

A  congested  liver  is  enlarged  and  pulsating. 

Spleno-medullary  leukemia. 

Hematemesis  and  epistaxis  are  the  two  most  frequent 
forms  of  hemorrhage. 

A  profuse  hemorrhage  reduces  the  size  of  the  spleen. 

Though  intestinal  hemorrhage  is  uncommon  a  severe 
diarrhea  will  nevertheless  reduce  the  size  of  the  spleen. 

Splenic   anemia. 

Hematemesis  is  very  common  and  is  also  associated 
with  splenomegaly. 

The  liver  may  subsequently  be  involved  in  a  second- 
ary cirrhosis  which  of  itself  causes  further  hemorrhage, 
ascites,  jaundice,  etc. 

Malarial   cachexia. 

In  malarial  cachexia  which  follows  repeated  attacks 
of  any  of  the  malarial  fevers,  fatal  attacks  of  hema- 
temesis may  occur. 

The  spleen  is  enormously  enlarged.  (Ague-cake 
spleen.) 

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The  hemorrhages  and  the  parasites  cause  severe 
secondary  anemia. 

Retinal  hemorrhages   very   common. 
Yellow  fever. 

Black  vomit  occurs  on  third  day  during  the  rising 
course  of  the  fever  and  a  synchronous  decline  of  the 
pulse  rate — which  is  a  peculiar  combination.  Hema- 
temesis  may  reoccur  during  the  secondary  fever. 

DIFFERENTIAL  DIAGNOSIS. 


HEMATEMESIS 


1.  Previous  history  points 
to  gastric,  hepatic  or  splenic 
disease. 

2.  The  blood  is  brought  up 
by  vomiting,  prior  to  which 
the  patient  may  experience  a 
feeling  of  giddiness  or  faint- 
ness. 

3.  The  blood  is  usually 
clotted,  mixed  with  particles 
of  food  and  has  an  acid  re- 
action. 

4.  Subsequent  to  the  at- 
tack the  patient  passes  tarry 
stools  and  signs  of  disease  of 
the  abdominal  viscera  may  be 
detected. 


HEMOPTYSIS. 


1.  Cough  or  signs  of  some 
pulmonary  or  cardiac  disease 
precedes  the  hemorrhage. 

2.  The  blood  is  coughed  up 
and  is  usually  preceded  by  a 
sensation  of  tickling  in  the 
throat.  If  vomiting  occurs, 
it  follows  the  coughing. 

3.  The  blood  is  frothy, 
bright  red  in  color,  alkaline  in 
reaction.  If  clotted,  rarely  in 
such  large  coagula  and  muco- 
pus  may  be  mixed  with  it. 

4.-  The  cough  persists, 
physical  signs  of  local  dis- 
ease in  the  chest  may  be  de- 
tected. The  sputa  may  be 
blood-tinged  for  several  days. 


HEMOPTYSIS. 

DEFINITION. 

A  symptom  denoting  coughing  up  of  blood. 

CAUSES. 

1.     PULMONARY. 

(a)      TUBERCULOSIS. 

May  occur  at  any  stage  of  the  disease. 

In  fact,  a  brisk  hemorrhage  may  be  the  first 
symptom  to  lead  us  to  examine  the  lungs.  In  these 
cases  we  will  find  pulmonary  signs  quite  marked,  al- 
though only  one  hemorrhage  has  occurred. 


104 


Repeated  attacks  usually  occur  at  any  time  with 
or  without  cause. 

The  amount  of  blood  lost  varies  from  blood- 
tinged  sputa  to  cup  fulls. 

It  seems  paradoxical  to  state  that  many  tuber- 
cular patients  stand  these  losses  of  blood  well  as 
evidenced  by  the  temporary  improvement  in  the 
dyspnea,  chest  oppression  and  cough.  Repeated  at- 
tacks, however,  cause  depression. 

If  the  hemorrhage  be  follow^ed  by  persistent 
rise  in  fever  or  by  the  appearance  of  fever  where 
none  has  previously  existed,  it  means  that  the  de- 
struction of  lung  tissue  is  going  on  rapidly. 

A  purulent  sputum  intimately  admixed  with 
blood  is  very  frequent  and  is  diagnostic  of  cavity 
formation. 

(b)  PNEUMONIA. 

The  usual  history  is  that  a  blood-tinged  sputum 
becomes  manifest  within  24  hours  after  the  initial 
congestive  chill. 

In  some  cases  a  free  hemorrhage  may  mark  the 
onset  of  the  disease. 

The  sputum  is  extremely  viscid  and  tenacious. 

The  admixture  of  the  blood  and  viscid  mucus 
is  called  "prune-juice"  expectoration. 

Although  R.  B.  C.  may  be  found  intact  in  the 
sputum,  the  largest  proportion  is  found  dissolved 
in  the  sputum  thereby  giving  the  sputum  a  "rusty" 
color. 

In  some  cases  a  simple  catarrhal  exudate  is 
found  throughout  the  entire  course  of  lobar  pneu- 
monia. 

(c)  Abscess,  gangrene,  cancer  and  syphilis  of  lung. 

(d)  Pulmonary  congestion    (including  hypostatic  conges- 
tion and  pulmonary  edema. 

In  these  cases  the  sputa  are  watery  and  blood- 
tinged  and  seldom  profuse. 

2.  CARDIAC.  With  failing  compensation  of  the  heart 
we  find  an  increase  in  mechanical  congestion  of  the 
lung.  Expectoration  then  becomes  decidedly  blood- 
streaked. 

105 


Pulmonary  engorgement  occurs  earlier  in  mitral 
than  in  aortic  disease.  In  fact,  it  is  seldom  seen  in 
aortic  regurgitation. 

ARTERIAL. 

Thoracic  aneurism.  According  to  Osier,  the  bleed- 
ing may  have  its  origin  from: 

(a)  Soft  granulations  in  the  trachea  at  point  of 
compression,  in  which  cases  the  sputa  are  blood- 
tinged. 

(b)  Rupture  of  the  aneurismal  sac  into  the  trachea 
or  bronchi, 

(c)  Perforation  into  lung  or  erosion  of  lung  tissue. 

The  bleeding  may  be  profuse,  rapidly  proving 
fatal  and  is  a  common  cause  of  death. 

It  may  persist  for  weeks  or  months,  in  which 
cases  it  is  a  hemorrhagic  weeping  through  the 
sac  which  is  exposed  in  the  trachea. 

Death  from  hemorrhage  is  relatively  more 
common  in  aneurism  of  the  third  portion  of  the 
arch  and  of  the  descending  aorta. 

According  to  Broadbent,  the  aneurism  of 
"physical  signs"  springs  from  the  ascending 
aorta  while  the  aneurism  of  "symptoms"  springs 
from  the  transverse  arch. 

Rarer  causes. 

(a)  Ulcerative  affections  of  larynx,  trachea  or 
bronchi. 

(b)  Vicarious  menstruation. 

(c)  Gout. 

(d)  Purpura  hemorrhagica. 


HEMATURIA. 

DEFINITION. 

Blood  in  the  urine.    It  is  a  symptom  and  not  a  disease. 

CAUSES. 

1.      RENAL. 

(a)  Stone  in  kidney. 

(b)  Tuberculosis. 

(c)  Tumors. 

(d)  Inflammations. 

lOfi 


Acute  Bright's. 

Acute  exacerbations  of  chronic   Bright's. 

Septic  nephritis, 

(e)  Congestion. 

(f)  Chemicals:    turpentine,  carbolic,  cantharides,  etc. 

(g)  Infarction  as  in  septic  endocarditis, 
(h)     Injury  to  loins. 

(i)      Parasites. 

Filaria  sanguinis  hominis. 
Bilharzia. 

2.  URETERAL  CAUSES. 

(a)     During  passage  of  stone  in  ureter. 

3.  VESICAL  CAUSES. 

(a)  Stone  in  bladder. 

(b)  Tumors. 

(c)  Ulcer  of  mucosa:  usually  tubercular. 

(d)  Hemorrhagic  cystitis. 

4.  URETHRAL  CAUSES. 

(a)  Gonorrhea. 

(b)  Dilatation  of  stricture  and   meatotomy. 

(c)  False  passage  with  instrument. 

(d)  Stone. 

(e)  Papilloma  and  urethral  caruncle. 

(f)  Fracture  of  pelvis. 

(g)  Ulceration  and  fissure  at  bladder  neck. 

5.  PROSTATIC  CAUSES. 

(a)  Enlarged  prostate. 

(b)  Hard  small  fibrous  prostate  with  erosion  of  blad- 
der mucus  membrane. 

6.  INFECTIOUS  FEVERS.     Especially  scarlatina. 

7.  MALARIA. 

8.  LEUKEMIA. 

LOCALIZING  THE  SOURCE  OF  THE    HEMATURIA. 

Only  by  direct  examination  with  the  urethroscope  and 
the  cystoscope  and  by  ureteral  catheterization  can  we 
localize  the  source  of  bleeding  with  absolute  certainty. 

107 


SPECIAL    REMARKS   ON    INDIVIDUAL   DISEASES. 
Tuberculosis  of  the  kidney. 

Hematuria  appears  at  irregular  intervals  without  as- 
signable cause.     It  is  never  profuse. 

Color  of  urine  is  milky  white  due  to  presence  of  pus. 
A  sterile  urine  with  a  lot  of  pus.  Urine  is  acid  and  con- 
tains tubercle  bacilli. 

Increased  frequency  of  urination  both  day  and  night 
even  before  implication  of  bladder.     Polyuria. 

Renal  tuberculosis  is  at  first  a  unilateral  disease. 

Bladder  always  becomes  secondarily  involved.  Cysto- 
scopy reveals  ulcerations  usually  around  the  vesico-ure- 
thral  orifices  and  trigone  and  the  ureteral  openings.  Con- 
gestions of  the  ureteral  papillas  are  typical  and  show 
ulcerations  and  hemorrhages. 

Symptoms  of  cystitis  soon  develop. 
Acute  Bright's  Disease. 

Free  blood  in  the  urine  gives  the  urine  a  "smoky" 
color. 

Marked  reduction  in  urinary  output. 

Associated  with  the  blood  we  find  various  forms  of 
casts:   blood,  hyaline,  granular  and  epithelial. 

Anemia  and  dropsy  are  associated  characteristic  fea- 
tures. 

Passive  congestion  of  tlie  kidney. 

Hematuria  appears  for  a  prolonged  period;  is  seldom 
large  in  amount  and  usually  associated  with  some  diminu- 
tion in  urinary  output. 

Malignant  disease  of  the  kidney. 

Hematuria  appears  and  disappears  suddenly  without 

any  assignable  cause. 

Bleeding  persists  in  spite  of  any  treatment. 

It  occurs   as   an   early  manifestation   of  the   disease. 

Renal  calculus. 

While  bleeding  usually  occurs  at  the  time  when  the 
stone  migrates  it  may  occur  at  any  time. 

During  the  attack  of  colic,  excruciating  pains  are 
felt  in  the  loin  and  extend  into  the  testicle  and  to  inner 
side  of  the  thigh.  After  the  attack  a  smoky  urine  is 
voided. 

108 


During  the  intervals  between  the  attack  both  pus  and 
blood  will  appear  if  the  kidney  has  become  involved  in 
a  suppurative  inflammation. 
Vesical  Calculus. 

Hematuria  is  an  intermittent  and  not  a  constant  and 
is  almost  invariably  small  in  amount. 

A  few  drops  may  be  squeezed  out  at  the  end  of  urina- 
tion or  the  blood  may  be  mixed  with  the  urine. 

The  associated  symptoms  are  day  frequency,  pains 
which  are  referred  to  the  glans  penis,  stoppage  of  the 
urine  while  in  full  stream  and  inflammation  of  the  bladder 
(cystitis). 

TESTS  FOR  BLOOD  IN  THE   URINE. 

1.  Microscopical.  Centrifuge  the  urine  and  examine  a 
portion  of  the  sediment  for  small  circular  discs  which 
are  more  regular  in  form  than  any  of  the  other  mor- 
phological elements  of  the  urine.  They  are  non-gran- 
ular and  non-nucleated  and  smallest  of  the  formed  ele- 
ments. 

2.  Gualac  test. 

Stratify  some  urine  upon  an  equal  mixture  of  ozon- 
ized oil  of  turpentine  and  a  1%  alcoholic  tincture  of 
guaiacum. 

A  bluish  ring  appears  at  the  junction  of  these 
liquids  if  blood  be  present. 

Pus  also  gives  a  positive  reaction  but  the  ring 
disappears  on  boiling. 

All  urine  before  testing  must  be  acid.  If  not, 
make  it  so  by  adding  acetic  acid. 

3.  Julius  Von  Kossa's  Test.     (See  p.  89.) 

Sometimes,  instead  of  tiny  red  hemoglobin  drop- 
lets a  rose-colored  ring  appears  above  the  surface  of 
the  chloroform.  In  such  cases,  decant  the  supernatent 
liquid  and  add  a  few  more  c.c.  of  alcohol  and  then 
the  red  droplets  will  appear. 

HEMATURIA    MUST    BE    DISTINGUISHED 
FROM    HEMOGLOBINURIA. 

In   hematuria   R.   B.    C.   are   found   but  not   in  hemo- 
globinuria.    Each  has  a  specific  absorption  spectrum. 

109 


HEMORRHAGE  INTO  THE  BRAIN. 

MENINGEAL  OR  RIAL  HEMORRHAGE. 

Most  frequent  causes  are  fracture  of  the  skull  (usu- 
ally over  the  anterior  inferior  angle  of  the  parietal  bones) 
involving  the  middle  meningeal  artery,  and  secondly  rup- 
ture of  miliary  aneurisms. 

The  blood  may  be  extra-  or  intradural. 

In  the  latter  instance,  the  blood  finds  its  way  into 
the  subarachnoid  space,  therefore  lumbar  puncture  should 
yield  a  bloody  fluid. 

Typical  diagnostic  symptoms  are  absent  though  they 
may,  to  some  extent  resemble  those  of  intracranial  hemor- 
rhage. The  symptoms  depend  upon  the  size  and  location 
of  the  hemorrhage. 

Paralyses  are  usually  absent. 

Meningeal  hemorrhage  is  the  cause  of  50%  of  all 
still-births.  This  may  usually  be  explained  by  prolonged 
labors,  instrumental  delivery,  etc. 

In  those  cases  where  the  child  survives,  idiocy  may 
subsequently  manifest  itself. 

INTRACEREBRAL  HEMORRHAGE. 

Hemorrhage   takes    place    into    the    brain    substance. 

The  i|;iost  frequent  location  is  in  the  neighborhood  of 
the  Circle  of  Willis  at  the  base  of  the  brain.  The  len- 
ticulo-striate  artery  suffers  most. 

The  cortical  vessels  are  not  as  often  affected  as  the 
central  arteries. 

These  hemorrhages  are  of  the  concealed  variety  and 
although  small  in  amount  is  attended  by  grave  symptoms 
because  the  cranial  cavity  is  compromised  and  pressure 
increased. 

The  symptoms  of  a  "stroke"  are  given  in  the  differ- 
ential  diagnostic   table  on  page  112. 

The  abrupt  onset  is  due  to  sudden  compression  of  the 
brain. 

The  paralysis  is  due  to  the  destruction  of  the  motor 
area  or  any  part  of  the  pyramidal  tract. 

Only  the  lower  part  of  the  face  is  involved  as  com- 
pared to  the  entire  side  of  the  face  in  Bell's  palsy. 

110 


The  face  is  involved  on  the  same  side  as  the  arm  and 
the  leg  owing  to  the  decussation  of  the  upper  motor  seg- 
ment^of  the  facial  nerve.    The  arm  is  more  paralyzed  than 

Crossed  paralysis  means  that  the  lesion  is  in  the 
crus,  pons  or  medulla,  i.  e.,  there  is  a  paralysis  of  a  cere- 
bral nerve  on  one  side  with  a  loss  of  powder  (or  sensa- 
tion)  on  the  other  side. 

^  When  hemianesthesia  is  marked  the  lesion  is  usually 
m  the  internal  capsule  (posterior  limb). 

Emboli  in  cases  of  ulcerative  endocarditis  usually 
enter  the  left  carotid  artery  and  then  carried  to  the  cere- 
bral arteries  so  that  certain  focal  symptoms  may  occur: 

Left  middle  cerebral  artery;  hemiplegia  with  aphasia. 

Vertebral  artery:     acute  bulbar  paralysis. 

Basilar:  double  hemiplegia  with  bulbar  symptoms 
because  of  its  relation  to  the  pons. 

Posterior  cerebral:    hemianopia  and  sensory  aphasia. 


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113 


UTERINE  HEMORRHAGE. 
Menorrhagia  and  Metrorrhagia. 

DEFINITION. 

Bleeding  from  the  womb  may  occur  either  at  the 
normal  menstrual  period  or  at  any  time  between  the 
menses. 

Menorrhagia.    Excessive  menstrual  bleeding. 
Metrorrhagia.     Bleeding  between  periods. 

CAUSES.     A  majority  of  the  cases  occur  in  connection  with 
labor  and  abortion. 

1.  Abortion    and    miscarriage.       (Retained    secundines; 
placental  tissue.) 

2.  Subinvolution  of  uterus,  the  result  of  post-abortive  or 
puerperal  infection. 

3.  Chronic  endometritis.     (Fungosities.) 

4.  Backward  displacement  of  the  womb. 

5.  Uterine  tumors. 

(a)  Polypi. 

(b)  Fibroid    (only   when   endometrium   is   involved). 

(c)  Cancer. 

6.  Ovarian  and  tubal  disease. 

7.  Impeded  circulation  as  a  result  of  cardiac,  pulmonary 
or  hepatic  disease. 

8.  Menopause.     (Suspicious  of  cancer.) 

9.  Postpartum  hemorrhage. 

10.  Lacerations  of  cervix,  vagina  or  perineum. 

11.  Placenta  previa. 

12.  Ectopic    pregnancy.      (Concealed   hemorrhage.) 

13.  Inversion  of  the  uterus. 

14.  Tuberculosis  and  syphilis  of  the  uterus. 

SPECIAL    REMARKS. 
Menstruation. 

1.  A  periodic  phenomenon  occurring  monthly  beginning 
in  girls  at  about  the  13th  year. 

2.  Each  girl  soon  develops  a  certain  "standard."     That  is 
to  say,  that  she  flows  a  certain  number  of  days,  uses 

114 


a  certain  number  of  napkins  and  has  a  certain  amount 
of  pain,  etc.  Any  deviation  later  in  life  from  this 
standard  means  some  abnormality. 

3.  The  flow  is  most  abundant  at  the  onset.  It  is  vari- 
ously estimated  from  2  to  8  ounces. 

4.  The  average  duration  of  the  menstrual  flow  is  4  days. 

5.  Menstrual  blood  is  dark  in  color,  alkaline  in  reac- 
tion, not  coagulable  due  to  presence  of  mucus  and 
contains  epithelial  cells.  Prior  to  the  appearance  of 
the  flow  and  for  a  few  days  after  the  flow  has  stopped, 
mucus  is  very  abundant. 

6.  Dysmenorrhea.     Excessive  pains  during  menstruation. 

7.  The  most  frequent  causes  of  prolonged  menstruation 
are:  polypoid  endometritis,  retroversion,  subinvolu- 
tion and  uterine  tumors. 


115 


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116 


Chronic    Endometritis. 

In  consequence  to  a  long-standing  congestion  from 
whatever  cause,  the  lining  membrane  of  the  womb  is 
stimulated  to  excessive  activity  with  the  formation  of 
polypi  or  fungosities. 

These  fungosities  are  directly  responsible  for  the 
large  amount  of  blood  lost  and  for  the  prolongation  of  the 
menstrual  period. 

This  chronic  engorgement  further  incites  connective 
tissue  hypertrophy  in  the  uterine  musculature,  with  the 
result  that  the  uterus  becomes  enlarged. 

The  other  symptoms  of  this  condition  are   obscured 
by    the    underlying    pathological    cause    (which    may    be 
displacements,  fibroids,   lacerations  of  cervix,   gonorrhea, 
etc.). 
Retroversion  of  Uterus. 

Chronic  congestion  of  the  womb  resulting  from  back- 
ward displacement  of  this  organ  results  in  menorrhagia 
and   dysmenorrhea. 

The  other  diagnostic  symptoms  are:  tenesmus,  pain- 
ful defecation,  intermenstrual  pain  due  to  prolapse  of 
the  ovaries. 

By  bimanual  palpation,  the  cervix  will  be  found  low 
down  and  anteriorly  placed.  The  fundus  cannot  be  pal- 
pated through  the  abdomen. 

Uterine    Fibroids. 

Hemorrhage  occurs  only  when  the  tumor  involves  the 
endometrium. 

Hemorrhage  is  therefore  profuse  in  cases  of  sub- 
mucus  fibroids.  The  usual  term  applied  to  these  fibroids 
is  "polypi." 

Polypi  tend  to  increase  the  surface  area  of  the  endo- 
metrium thus  creating  a  larger  bleeding  surface. 

In  addition  to  menorrhagia  we  have  metrorrhagia 
which  is  quite  pronounced. 

Interstitial  or  intramural  fibroids  also  cause  metror- 
rhagia but  the  subperitoneal  variety  does  not. 

When  these  polypoid  masses  obstruct  the  cervical 
canal  we  will  find  symptoms  of  obstructive  dysmenorrhea 
and  intermenstrual  pain. 

Uterine  Cancer. 

Irregular,  atypical  bleedings  at  the  climacteric  are 
suspicious  symptoms. 

117 


Pain  and  foul  discharge  are  late  symptoms. 

A  lacerated,  indurated  and  eroded  cervix  which  bleeds 
easily  when  touched  and  is  firmly  attached  to  the  under- 
lying structures  is  very  suspicious  of  malignant  disease. 

Post-Partum   Hemorrhage. 

1.  While  bleeding  after  delivery  may  come  from  the  cer- 
vix, perineum  or  vagina,  we  restrict  the  usage  of 
this  term  to  hemorrhage  from  the  placenta!  site. 

2.  Post-partum  hemorrhages  usually  occur  within  the 
first  24  hours  after  delivery. 

3.  The  hemorrhage  may  be  visible  or  invisible.  When 
invisible  the  blood  collects  within  the  womb  greatly 
distending  it  (hematoma). 

4.  The  uterus  is  soft  and  flabby,  A  strongly  contracted 
uterus  is  positive  evidence  against  post-partum  hemor- 
rhage. 

5.  Predisposing  causes  are:  protracted  labors,  injudicious 
use  of  anesthetics,  hurried  deliveries  with  or  without 
use  of  pituitrin  or  instruments.  Also  hurried  de- 
liveries of  the  placenta. 


EPISTAXIS. 

DEFINITION. 

Bleeding  from  the  nose. 

LOCAL    CAUSES. 

1.  TRAUMATISM. 

(a)  Blows  on  the  nose. 

(b)  Picking  the  nose  causes  the  erosion  of  a  thin- 
walled  blood  vessel  on  the  cartilage  of  the  sep- 
tum just  within  the  anterior  nares  about  % 
of  an  inch  above  the  floor  of  the  nose. 

(c)  Indirectly  in  fracture  of  the  base  of  the  skull. 

(d)  Operations  on  nose. 

2.  SPECIFIC  ULCERATIONS. 

(a)  Syphilitic. 

(b)  Tubercular. 

(c)  Malignant. 

3.  ANGIOMATA.     (Bleeding  polypi  on  septum,) 

118 


4.  ADENOIDS.  Children  who  have  adenoids  are  subject 
to  epistaxis  and  repeated  attacks  of  "cold  in  the 
head." 

By  making  a  digital  examination  of  the  naso- 
pharynx, the  finger,  when  withdrawn,  with  be  coated 
with   a   thick  white-of-egg-like   mucus   and   blood. 

5.  FOREIGN    BODY   IN    NOSE. 

The  presence  of  a  one-sided  hemorrhage  asso- 
ciated with  a  muco-purulent  discharge"  in  a  child  is 
suspicious  of  the  presence  of  a  foreign  body  in  the 
child's  nose. 

CONSTITUTIONAL  CAUSES. 

1.  As  a  diagnostic  prodrome  of  typhoid. 

2.  In  many  conditions  associated  with  an  increased  pulse 
tension  as  in  cardiac,  vascular  and  renal  diseases. 
In  the  aged  it  is  often  a  precursor  of  cerebral  hemor- 
rhage. 

3.  Hemophilia,  scurvy  and  purpura. 

4.  Vicarious  menstruation. 

MELCENA— ENTERRHAGIA. 
DEFINITION. 

Bloody  stools  or  hemorrhage  from  the  bowels. 

ETIOLOGY. 

1.  Diseases  of  the  rectum. 

(a)  Hemorrhoids.      (Internal   and  external.) 

(b)  Anal  fissure. 

(c)  Cancer. 

(d)  Fistulo-in-ano. 

2.  Gastric  and  duodenal   ulcer. 

3.  Atrophic  cirrhosis  of  liver. 

4.  Intussusception. 

5.  Ulcerations  of  the  bowel. 

(a)  Syphilis. 

(b)  Typhoid. 

(c)  Cancer. 

(d)  Dysentery. 

(e)  Tuberculosis. 

(f)  Ischio-rectal  abscess  breaking  through  the  bowel. 

6.  Severe  enteritis.     (Very  rare.) 

119 


DIAGNOSIS. 

It  is  very  apparent  that  from  the  above  enumerated 
causes  that  blood  appearing  at  the  anal  orifice  may 
originate  from  any  portion  of  the  gastro-intestinal  tract. 
As  a  general  rule,  it  may  be  stated,  that  when  the 
bleeding  is  high  up,  as  for  instance  in  the  stomach  and 
in  the  duodenum,  the  blood  is  never  bright  red  in  color 
but  a  black,  tarry  or  coffee  color.  The  black  color  is  due 
to  ferrous  sulphide. 

If  the  blood  be  adherent  to  scybalous  masses  or  to 
v^ell  formed  feces,  it  is  usually  derived  from  the  rectum 
or  anus  and  indicates  piles. 

If  it  be  evenly  distributed  with  the  food  material  and 
brown  in  color,  it  indicates  hemorrhage  in  the  stomach 
or  high  up  in  the  smaller  bowels,  especially  if  the  stood 
be  solid. 

If  evenly  mixed  with  liquid  stools  the  colon  is  usually 
the  site  of  the  bleeding. 

It  is  useless  to  search  for  red  cells  in  the  feces  ex- 
cept in  cases  of  profuse  hemorrhage. 

The  chemical  tests  for  occult  blood  are:  guaiac  test, 
Weber's  test,  Adler's  benzidin  test,  etc. 

SPECIAL   REMARKS. 

Constipation  is  a  great  predisposing  cause  in  the 
development  of  piles  and  at  the  same  time,  the  passage 
of  hardened  feces  over  these  blood  tumors  is  very  apt  to 
favor  rupture  thereof,  especially  when  straining.  Conse- 
quently bleeding  results.  Repeated  hemorrhages  may  re- 
sult in  severe  secondary  anemia. 

In  atrophic  cirrhosis  we  find  a  diagnostic  combination 
of  bowel  hemorrhages  and  hemorrhoids  in  consequence 
of  the  existing  portal  congestion.  It  is  especially  so  in 
topers.  In  these  cases,  intestinal  hemorrhages  usually 
follow  attacks  of  hematemesis.  But,  hemorrhages  from 
the  bowels  may  occur  for  several  years  without  hema- 
temesis. 

In  intussusception  blood  may  appear  in  the  stools 
spontaneously  or  after  an  enema  has  been  administered. 
It  is  usually  mixed  with  mucous.  In  children,  the  exist- 
ence of  a  bloody  and  mucous  diarrhea  associated  with  a 
palpable  abdominal  tumefaction  and  severe  tenesmus  is 
very  diagnostic  of  telescoping  of  the  bowel. 

120 


A  free  intestinal  hemorrhage  may  occur  as  a  com- 
plication in  typhoid  fever.  It  seems  strange  that  such 
hemorrhages  may  not  be  attended  by  bad  effects.  Usually 
occurs  during  the  second  or  third  weeks.  It  may  be  sus- 
pected if  there  be  a  progressive  decline  in  the  fever  or  in 
blood  pressure.  It  usually  comes  on  suddenly.  Fatal 
collapse  may  sometimes  supervene  before  the  blood  ap- 
pears in  the  evacuations.  In  some  cases,  a  slight  hemor- 
rhage may  antecede  a  fatal  hemorrhage.  The  bleeding 
arises  from  the  sloughing  ulcers  on  Payer's  patches. 

In  both  forms  of  dysentery  we  find  a  history  of  bloody 
stools  at  one  time  or  other.  Usually  the  stools  are  watery 
and  blood  streaked,  but  a  pure  bloody  stool  may  also 
occur.  Mucous  may  appear  before  the  blood.  Tenesmus 
is  very  characteristic. 

Pus  in  association  with  blood  in  the  stools  usually 
signifies  ulcerations  in  the  bovv'els  but  it  is  not  very  exces- 
sive. When  considerable  pus  appears  in  the  stools  it 
usually  signifies  that  a  neighboring  abscess  has  ruptured 
into  the  bowels. 

Cancer  of  the  rectum  and  malignant  disease  of  the 
bowels  are  invariably  accompanied  by  pus  and  blood  in 
the  bowels. 

GUAIAC  TEST  for  blood  in  the  feces. 

1.  Rub  up  a  small  portion  of  the  stools  with  water  and 
then  place  same  in  a  test  tube. 

2.  Add  glacial  acetic  acid  (Vs  of  the  above  volume). 

3.  Shake  vigorously  and  add  a  few  c.c.  of  ether. 

4.  Shake  thoroughly  again  and  allow  to  settle.  (If  blood 
be  present,  the  ether  takes  on  a  brownish  color.  And, 
if  the  ethereal  extract  be  not  clear,  add  a  few  drops 
of  alcohol.) 

5.  Stratify  upon  this  ethereal  extract  a  mixture  of  equal 
parts  of  fresh  tincture  guaiacum  and  ozonized  oil  of 
turpentine  and  a  blue  contact  ring  appears. 

Note. — This  is  a  good  negative  test.     Meat  must 
be  excluded  from  the  diet. 

WEBER'S  TEST  for  blood  in  feces. 

1.  A  small  portion  of  the  stool  is  extracted  with  ether 
in  order  to  remove  the  fat.  Then  it  is  separated  from 
the  ethereal  solution, 

121 


2.  Rub  up  this  fat-free  feces  with  water  and  proceed 
as  in  the  guaiac  test  as  stated  under  statements 
2  and  3. 

3.  The  ether  takes  up  the  hematin  wliich  can  he  detected 
by  its  absorption  bands  with  the  spectroscope. 

(a)  An    intense    narrow    band    in    the    red    between 
C  and  D. 

(b)  A  group  of  three  broader  bands: 
(x)     One  in  the  yellow. 

(y)  One  in  the  boundary  line  between  the  yel- 
low and  the  green. 

(z)  One  at  the  boundary  between  the  green  and 
the  blue.     This  one  is  difficult  to  recognize. 

Note. — A  very  reliable  and  sensitive  test. 

In  order  to  avoid  any  confusion  with  the  spectrum 
given  by  methemoglobin  or  by  chlorophyll  add  al- 
coholic potassium  hydrate,  water  and  ammonium  sul- 
phide solution  which  reduces  hematin  to  hemochro- 
mogen.     This  gives  two  bands  in  the  green. 

ADLER'S  BENZIDINE  TEST. 

1.  Extract  the  stool  with  a  mixture  of  alcohol  and  ether. 

2.  Treat  with  glacial  acetic  acid.     (Vs  of  its  volume.) 

3.  Shake  thoroughly,  allow  to  settle.  If  blood  be  present 
the  ether  becomes  brownish  in  color. 

4.  This  acid  ethereal  extract,  which  now  contains  the 
hematin,  is  treated  with  2  c.c.  of  a  saturated  alcoholic 
benzidine  solution  and  2  c.c.  of  3%  peroxide  of  hy- 
drogen. 

In  the  presence  of  blood  an  intense  green  color 
appears. 

It  will  recognize  blood  in  the  proportion  of  one 
part  blood  to  100,000  parts  water. 

It  is  chiefly  valuable  as  a  negative  test. 

Hemoglobin  must  be  removed  from  diet.  The 
same  can  be  said  about  prunes. 


122 


ECTHOL. 

A  vegetable  product;   each  teaspoon  containing: 

Thuja  Occidentalis  3  grains 

Echinacea  Angustifolla 28  grains 

Local  Action.     An  astringent  antiseptic. 

Indicated  in  inflammations  of  the  skin,  especially 
purulent  inflammations  like  boils,  carbuncles,  abscess, 
erysipelas,  mammitis,  chancroid,  ulcers  and  infected  cuts. 

It  should  be  applied  undiluted  for  topical  applications. 
All  collections  of  pus  must  first  be  incised  and  then 
washed  with  Ecthol. 

It  is  not  an  antiseptic  in  the  ordinary  sense  of  the 
word  but  by  its  direct  action  upon  the  cells  it  stimulates 
them  to  overcome  bacterial  growth  and  aids  in  promoting 
healing.     It  is  not  poisonous  like  many  other  antiseptics. 

Internal  or  Systemic  Action. 

In  many  diseases  due  to  infection  with  pathogenic 
bacteria,  especially  the  pyogenic  variety,  Ecthol,  which 
consists  of  two  vegetable  products,  heretofore  regarded 
as  alteratives,  apparently  stimulates  the  body  cells  to 
greater  activity  so  that  more  opsonins  are  poured  out 
into  the  blood,  thus  endeavoring  to  overcome  the  effects 
of  the  invading  germs. 

It  may  therefore  be  used  in  many  blood  disorders  as 
a  systemic  antiseptic  and  a  resistance  promoter.  It  is 
recommended  for  internal  use  in  acne,  furuncle,  carbuncle, 
erysipelas,  pyelitis  and  especially  septicemia. 

Echinacea  is  also  credited  with  being  a  febrifuge. 
Ecthol  may  therefore  be  also  used  in  febrile  conditions. 

Dose. — One  teaspoon  3  or  4  times  a  day. 

BATTLE  CSi  CO., 

ST.  LOUIS,  MO. 


123 


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